eMedicine Specialties > Infectious Diseases > Fungal Infections

Pneumocystis (carinii) jiroveci Pneumonia: Treatment & Medication

Author: Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Coauthor(s): Frederick Burton Rose, MD, FACP, Professor, Department of Medicine, University Hospital Epidemiologist, State University of New York Upstate Medical University; Joseph C McLean, MD, Staff Physician, Department of Internal Medicine, William Beaumont Army Medical Center; Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium; Tanya S Schreibman, MD, Consulting Staff, Department of Internal Medicine, Bach and Godofsky; Michael Rigsby, MD, Director of HIV Care Program, VA Connecticut Healthcare System, West Haven Campus; Associate Professor, Department of Internal Medicine, Yale University School of Medicine
Contributor Information and Disclosures

Updated: Oct 10, 2008

Treatment

Medical Care

While officially classified as a fungal pneumonia, P carinii pneumonia (PCP) does not respond to antifungal treatment. Although a histopathologic demonstration of the organism is required for a definitive diagnosis, treatment should not be delayed. Pneumocystis organisms persist in the host for days to weeks after therapy is started, allowing time for completion of the appropriate workup.

  • Treatment depends on the degree of illness at diagnosis (see Medication).
  • Treatment is based on the alveolar-arterial gradient, which may be mild (<35 mm Hg), moderate/severe (35-45 mm Hg), or severe (>45 mm Hg).
  • Severe disease is also indicated by a room air pO2 of less than 70 mm Hg.

Consultations

Consultation with a pulmonologist is required for BAL.

Medication

The recommended duration of treatment for P carinii pneumonia (PCP) is 21 days in patients with HIV infection and 14 days for all other patients. Patients infected with HIV tend to have a higher organism burden and respond to treatment slower than patients without HIV infection and therefore require a longer duration of therapy.

  • Treatment of extrapulmonary manifestations is the same as that for other pneumonias.
  • Up to 10% of mild-to-moderate PCP cases fail to respond to antibiotic treatment because of lack of drug efficacy.
  • In patients without HIV infection, response to treatment should begin in 4-5 days.
  • In patients infected with HIV, the treatment response typically takes longer but should occur within the first 8 days.
  • If no response occurs within the expected time, an appropriate alternative regimen should be used.
  • Adding additional PCP medications to a current regimen only increases the risk of adverse drug reactions without improving the likelihood of a good outcome.

Antibiotic

Antibiotics are primarily recommended for treatment for mild, moderate, or severe PCP. Trimethoprim-sulfamethoxazole (TMP-SMX) has been shown to be as effective as intravenous pentamidine and more effective than other alternative treatment regimens.8 The parenteral route may be considered in patients who present with serious illness or in those with gastrointestinal side effects. TMP-SMX is the preferred initial therapy during pregnancy according to consensus guidelines. The patient's neonatologist should be informed if the medication is used near delivery because of potential for hyperbilirubinemia and kernicterus.

The combination of clindamycin and primaquine is likely to be more effective than intravenous pentamidine in the treatment of infections that are resistant to TMP-SMX.9,10


Primaquine phosphate

A member of the 8-aminoquinoline group. Binds to parasite DNA and causes a major disruption in the metabolic process of the parasite.

Adult

Moderate-to-severe disease: 15-30 mg PO qd for 21 d and clindamycin 900 mg IV q8h
Mild-to-moderate disease: 15-30mg PO qd for 21 d and clindamycin 600 mg IV q8h (or 300-450 mg PO q8h)

Pediatric

Not established

May reduce thyroxine efficacy; coadministration with quinacrine may increase toxicity

Documented hypersensitivity; G-6-PD deficiency (may cause fatal hemolysis); NADH methemoglobin reductase deficiency (may cause methemoglobinemia)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in G-6-PD deficiency and those with tendency to develop granulocytopenia; caution in systemic lupus erythematosus or rheumatoid arthritis


Trimetrexate (Neutrexin) and leucovorin (Wellcovorin)

A lipid soluble derivative of methotrexate. One study showed it to be less effective but better tolerated than TMP-SMX in hospitalized patients with severe PCP. Inhibits dihydrofolate reductase, inhibiting bacterial growth. Given with leucovorin to attenuate bone marrow suppression.

Adult

45 mg/m2 IV (over 60-90 min) qd for 21 d and leucovorin (folinic acid) 20 mg/m2 IV or PO for 24 d (continue for 3 d after trimetrexate)

Pediatric

Not established

Increases toxicity of yellow fever vaccine; decreases effect of pneumococcal vaccine; erythromycin, rifampin, rifabutin, ketoconazole, and fluconazole may alter serum trimetrexate levels; cimetidine can decrease trimetrexate metabolism and cause an increase in trimetrexate levels; acetaminophen may compete for sulfate metabolites, causing changes in concentration of trimetrexate metabolites; clotrimazole, ketoconazole, and miconazole may increase trimetrexate plasma levels

Documented hypersensitivity; severe myelosuppression

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

To avoid potentially life-threatening toxicities, administer concurrently with leucovorin; caution in renal or hepatic dysfunction and mild myelosuppression


Trimethoprim-sulfamethoxazole (TMP-SMX, Bactrim, Septra, Co-trimoxazole)

Inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid. This results in inhibition of bacterial growth.
Preferred initial therapy during pregnancy according to consensus guidelines. The patient's neonatologist should be informed if the medication is used near delivery because of potential for hyperbilirubinemia and kernicterus.

Adult

Intravenous: (TMP) 20 mg/kg/d, (SMX) 75-100 mg/kg/d IV divided tid/qid
Oral: 2 double-strength tab tid

Pediatric

<2 months: Do not administer
>2 months: 15-20 mg/kg/d PO tid/qid based on TMP

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Documented hypersensitivity; megaloblastic anemia due to folate deficiency; age <2 mo

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholics, elderly, those receiving anticonvulsant therapy, or those with malabsorption syndrome); hemolysis may occur in G-6-PD deficient individuals; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation


Pentamidine (Pentam-300)

Inhibits growth of protozoa by blocking oxidative phosphorylation and inhibiting incorporation of nucleic acids into RNA and DNA, causing inhibition of protein and phospholipid synthesis.

Adult

4 mg/kg/d IV/IM for 14-21 d; dilute in 50-250 mL of 5% dextrose solution and infused over at least 1 h

Pediatric

150 mg/m2/d IV for 5 d, followed by 100 mg/m2/d IV for 16 d

Coadministration with cidofovir increases risk of nephrotoxicity; concomitant use of foscarnet may decrease serum calcium level; risk of pancreatitis with zalcitabine may be additive; coadministration with other drugs that prolong QT interval (eg, dofetilide) increases risk

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse reactions in up to 70-80% of patients include nausea, cardiac arrhythmias, hyperkalemia, and nephrotoxicity; caution in diabetes mellitus (hypoglycemia and hyperglycemia), hypertension or hypotension, hepatic dysfunction, hypoglycemia, leukopenia, and thrombocytopenia


Atovaquone (Mepron)

A hydroxynaphthoquinone that inhibits mitochondrial electron transport chain by competing with ubiquinone at ubiquinone-cytochrome-c-reductase region (complex III). Inhibition of electron transport by atovaquone results in inhibition of nucleic acid and ATP synthesis in parasites and microorganisms.

Adult

750 mg PO bid ac

Pediatric

Treatment or prevention:
<13 years: Not established
>13 years: Administer as in adults

May increase zidovudine serum levels; coadministration with rifampin or rifabutin may decrease atovaquone levels; atovaquone may decrease levels of TMP-SMX

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in elderly persons and in those with hepatic and renal impairment; may cause skin rash, fever, and abnormal liver function test results


Clindamycin (Cleocin HCl)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys. Alternative therapy for mild, moderate, or severe disease. Given with primaquine.

Adult

Moderate-to-severe disease: 900 mg IV q8h and primaquine 15-30 mg PO qd for 21 d
Mild-to-moderate disease: 600 mg IV q8h (or 300-450 mg PO q8h) and primaquine 15-30mg PO qd for 21 d

Pediatric

Not established

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile


Dapsone (Avlosulfon)

Given with trimethoprim. Mechanism of action is similar to that of sulfonamides where competitive antagonists of PABA prevent formation of folic acid, inhibiting bacterial growth.

Adult

100 mg PO qd and trimethoprim 5 mg/kg PO tid

Pediatric

Not established

May inhibit anti-inflammatory effects of clofazimine; hematologic reactions may increase with folic acid antagonists, eg, pyrimethamine (monitor for agranulocytosis during the second and third months of therapy); probenecid increases dapsone toxicity; trimethoprim with dapsone may increase toxicity of both drugs; due to increased renal clearance, dapsone levels may significantly decrease when administered concurrently with rifampin; DDI (dideoxyinosine) may reduce antipneumocystic activity of dapsone

Documented hypersensitivity; known G-6-PD deficiency (may cause hemolysis in these patients)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include fever, rash, methemoglobinemia, hemolytic anemia, nausea, vomiting, hepatitis, headache, neuropathy, insomnia, aplastic anemia, and erythema multiforme; perform weekly WBC counts (first month), then monthly (6 mo), then semiannually (discontinue if significant reduction in platelets, leukocytes, or hematopoiesis observed)
Caution in methemoglobin reductase deficiency, G-6-PD deficiency (patients receiving >200 mg/d), or hemoglobin M because of high risk for hemolysis and Heinz body formation; caution in patients exposed to other agents or conditions capable of producing hemolysis (eg, infection, diabetic ketosis); phototoxicity may occur when exposed to UV light

Corticosteroid

These agents are used as adjunctive initial therapy only in patients with HIV infection who have severe PCP as defined by a room air arterial oxygen pressure of less than 70 mm Hg or an arterial-alveolar O2 gradient that exceeds 35 mm Hg. Adjunctive steroids are not recommended in patients without HIV infection. Microbial degradation and clearance may trigger further inflammation, which can provoke a severe inflammatory response in the lungs that often worsens after therapy is begun. Adjunctive corticosteroid therapy can blunt this inflammatory response, reduce deterioration of oxygenation, and reduce the incidence of respiratory failure.11,12


Prednisone (Deltasone, Orasone, Sterapred)

Consensus guidelines recommend beginning corticosteroids as early as possible in HIV patients with severe disease.
Adjunctive corticosteroids may be used with the same indications as in nonpregnant adults. The maternal fasting and postprandial serum glucose levels should be monitored if used in the third trimester because of increased risk of glucose intolerance.
Methylprednisolone may be substituted at 75% of dose below if parental administration preferred.

Adult

40 mg PO bid for 5 d, then 40 mg/d for 5 d, then 20 mg qd for 11 d (administer 30 min before TMP-SMX)

Pediatric

4-5 mg/m2/d or 1-2 mg/kg PO qd; taper over 2 wk as symptoms resolve

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral, connective tissue, fungal, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction; GI bleeding or ulceration; not recommended for treatment of non-HIV patients with severe PCP

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use

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References
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Further Reading

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Keywords

Pneumocystis carinii pneumonia, PCP, P carinii pneumonia, Pneumocystis jiroveci pneumonia, P jiroveci pneumonia, Pneumocystis pneumonia, PCP prophylaxis, PCP prevention, opportunistic respiratory infection, opportunistic pneumonia, HIV, AIDS

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Contributor Information and Disclosures

Author

Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Nicholas John Bennett, MB, BCh, PhD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Frederick Burton Rose, MD, FACP, Professor, Department of Medicine, University Hospital Epidemiologist, State University of New York Upstate Medical University
Frederick Burton Rose, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Joseph C McLean, MD, Staff Physician, Department of Internal Medicine, William Beaumont Army Medical Center
Joseph C McLean, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Tanya S Schreibman, MD, Consulting Staff, Department of Internal Medicine, Bach and Godofsky
Disclosure: Nothing to disclose.

Michael Rigsby, MD, Director of HIV Care Program, VA Connecticut Healthcare System, West Haven Campus; Associate Professor, Department of Internal Medicine, Yale University School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

Klaus-Dieter Lessnau, MD, FCCP, Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Harold L Manning, MD, Associate Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School
Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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