Download Pneumonia in Immunocompromised Host

Pneumonia in Immunocompromised Host:-
By :Samar mohammed El-Rewaney
Pharm D4
Group 3
Pneumonia in Immunocompromised Host:Pneumonia in an immunocompromised host describes a
lung infection that occurs in a person whose ability to fight
infection is greatly reduced.
Causes
People who are immunocompromised have a defective immune
response.
Because of this, they are susceptible to infections by germs that typically
do not cause disease in healthy people.
They are also more vulnerable to the usual causes of pneumonia, which
can affect anyone.
immunosuppression can be caused by:
•Bone marrow transplantation
•Certain medications (including steroids and those used to treat
cancer )
•HIV infection
•Leukemia
•Organ transplant
Symptoms of pneumonia
•Cough (may be dry or produce mucus-like, greenish, or pus-like sputum)
•Chills with shaking
•Easy fatigue
•Fever
•General discomfort, uneasiness, or ill feeling (malaise )
•Headache
•Loss of appetite
•Nausea and vomiting
•Sharp or stabbing chest pain that gets worse with deep breathing or coughing
•Shortness of breath
Other symptoms that may occur:
•Excessive sweating or night sweats
•Joint stiffness (rare)
•Muscle stiffness (rare)
•Swollen gland
PNEUMONIA IN IMMUNOCOMPROMISED PATIENTS
Host Defect
Disorders or Therapy Associated
Likely Pathogens
With Defect
Defective PMNs
Neutropenia
Acute leukemia, aplastic anemia, cancer
chemotherapy
Gram-negative bacteria,
Staphylococcus aureus,
Aspergillus sp, Candida sp
Defective chemotaxis
Diabetes mellitus
S. aureus, gram-negative
aerobes
Defective intracellular
killing
Chronic granulomatous disease
S. aureus
Defective alternative
pathway
Sickle cell disease
Streptococcus
pneumoniae,
Haemophilus influenzae
C5 deficiency
Congenital disorder
S. pneumoniae, S. aureus,
gram-negative bacteria
Host Defect
Disorders or Therapy
Likely Pathogens
Associated With Defect
Cell-mediated immuno
deficiency
(T-cell deficiency or
dysfunction)
Hodgkin lymphoma, cancer
chemotherapy, corticosteroid
therapy
Mycobacteria, viruses
(herpes simplex virus,
cytomegalovirus),
Strongyloides sp,
opportunistic
fungi (Aspergillus, Mucor,
Cryptococcus spp),
Nocardia sp, Toxoplasma
sp
AIDS
Pneumocystis jiroveci,
Toxoplasma sp,
cytomegalovirus, herpes
simplex
virus, opportunistic
fungi (Aspergillus, Mucor,
Cryptococcus spp),
mycobacteria
Host Defect
Disorders or Therapy
Likely Pathogens
Associated With Defect
Humoral
immunodeficiency
(B-cell deficiency or
dysfunction)
Multiple myeloma,
agammaglobulinemia
Selective deficiency: IgA, IgG, IgM
Hypogammaglobulinemia
S. pneumoniae, H.
influenzae,
Neisseria meningitidis
S. pneumoniae, H.
influenzae
P. jiroveci, cytomegalovirus,
S. pneumoniae, H.
influenzae
Treatment :• Oxygen administration
• Oxygen saturation and cardiac monitoring
• Empiric antimicrobial therapy
• Chest physiotherapy
Management of pneumonia in the immunocompromised patient
Antibiotic rationale :-
•Treatment must be initiated rapidly as disease progression can be swift.
•Empirical treatment must take into account:
Local pathogens and their resistance patterns
The possibility of pseudomonal infections
•The broad-range of potential pathogens including atypical pathogens
•In the HIV-positive patient, infections such as Pneumocystis carinii should be considered.
Medication:The 2 goals of pharmacologic therapy are eradication of infections and prophylaxis
against common pathogens in high-risk patients.
Consult the 2007 Infectious Diseases Society of America (IDSA)/Chest guidelines for
optimal care.
1- Inpatient, non-ICU treatment
* Respiratory fluoroquinolone
* Beta-lactam plus a macrolide
2- Inpatient, ICU treatment
* Beta-lactam plus either azithromycin or fluoroquinolone
*For community-acquired methicillin-resistant Staphylococcus aureus infection, add
vancomycin or linezolid
* For Pseudomonas infection, use an antipneumococcal, antipseudomonal beta-lactam
plus either ciprofloxacin or levofloxacin (750-mg dose) or beta-lactam plus an
aminoglycoside and azithromycin or a beta-lactam plus an aminoglycoside and an
antipneumococcal fluoroquinolone.
Special considerations
•HIV:
Medication choices should be based on CD4 count and should be made in consultation
with an infectious disease specialist.
•Elderly patients:
Moxifloxacin is associated with faster clinical recovery than levofloxacin.
•Vitamin C:
Some evidence suggests that in vitamin C–deficient persons supplementation can lower the
risk of pneumonia. Further study is needed; however, it is promising, as it has a low cost
and low risk.
•Cystic fibrosis:
Addition of tobramycin to an antipseudomonal semisynthetic penicillin (eg, carbenicillin,
ticarcillin, mezlocillin, piperacillin, azlocillin).
•Burn :•Selective oral decontamination in burn patients has been advocated in some burn
centers. Reduced oral carriage of organisms responsible for pulmonary infections is
speculated to account for a lower frequency of pneumonias in these patients.
•Drug pharmacokinetics in burn patients are complex and incompletely understood.
Broadly, treatment can be conceptualized into 2 groups:
*First 48-hour acute phase:
Protein-rich fluid is lost from intravascular space. This leads to hypovolemia and a
drop in cardiac output, which results in tissue hypoperfusion and a fall in renal
blood flow.
*Beyond 48 hours:
Complex changes frequently occur in drug metabolism at the level of the liver, and
renal function can be variable in these patients.
Pneumocystis jiroveci Pneumonia (PCP)
-Trimethoprim-sulfamethoxazole (TMP-SMX) is the treatment of choice (AI).
The dose must be adjusted for abnormal renal function.
Adding leucovorin to prevent myelosuppression during acute treatment is not
recommended because of questionable efficacy and some evidence for a higher failure rate
(DII).
Oral outpatient therapy of TMP-SMX is highly effective among patients with mild-tomoderate disease (AI).
Mutations associated with resistance to sulfa drugs have been documented, but
their effect on clinical outcome is uncertain.
Patients who have PCP despite TMP-SMX prophylaxis are usually effectively
treated with standard doses of TMP-SMX (BIII).
- Patients with documented PCP and moderate-to-severe disease,
as defined by room air pO2 <70 mm/Hg or arterial-alveolar O2 gradient >35
mm/Hg, should receive corticosteroids as early as possible, and certainly within
72 hours after starting specific PCP therapy (AI).
If steroids are started at a later time, their benefits are unclear, although the
majority of clinicians would use them in such circumstances for patients with
severe disease (BIII).
The preferred corticosteroid dose and regimen is prednisone 40 mg by mouth
twice a day for days 1 to 5, 40 mg daily for days 6 to 10, and 20 mg daily for days
11 to 21 (AI).
Methylprednisolone at 75% of the respective prednisone dose can be used if
parenteral administration is necessary.
Alternative therapeutic regimens include
1- dapsone and TMP for mild-to-moderate disease (BI)
(this regimen may have similar efficacy and fewer side effects than TMP-SMX but is
less convenient because of the number of pills)
2- primaquine plus clindamycin (BI)
(this regimen is also effective in mild-to-moderate disease, and the clindamycin
component can be administered intravenously for more severe cases; however,
primaquine is only available orally) .
3- intravenous pentamidine (AI)
(generally the drug of second choice for severe disease)
4- atovaquone suspension (BI)
(this is less effective than TMP-SMX for mild-to-moderate disease but has
fewer side effects); and (DI).
5- trimetrexate with leucovorin (BI)
(this is less effective than TMP-SMX but can be used if the latter is
not tolerated and an intravenous regimen is needed).
Leucovorin must be continued 3 days after the last trimetrexate
dose. The addition of dapsone, sulfamethoxazole, or sulfadiazine to
trimetrexate might improve efficacy on the basis of the sequential
enzyme blockade of folate metabolism, although no study data exist
to confirm this (CIII). Aerosolized pentamidine should not be used
for the treatment of PCP because of limited efficacy and more
frequent relapse
Core Pathogens
Pseudomonas Aeruginosa
Core Antibiotics
Ciprofloxacin or amikacin
PLUS either
An anti-pseudomonal beta-lactam/beta-lactamase inhibitor
(piperacillin/tazobactam), or
Ceftazidime or carbepenems (imipenem, meropenem)
Resistant Acinetobacter
species
Anti-pseudomonal cephalosporin (ceftazidime), or
imipenem/meropenem, or amikacin
MRSA*
Add vancomycin
Core Pathogens
Enteric Gram-negative
bacilli
Klebsiella species and
Escherichia coli
Core Antibiotics
3rd-generation cephalosporin
e.g. intravenous ceftriaxone,
or beta-lactam / beta-lactamase inhibitor
e.g. intravenous ampicillin-sulbactam or
amoxicillin-clavulanic acid,
or quinolone
e.g. ciproflaxin.
Also, Staphylococcus aureus
Hemophilus influenzae and
Consider adding cloxacillin or clindamycin.
Streptococcus pneumoniae
Consider adding azithromycin or clarithromycin
Alternative to above: newer quinolone as monotherapy.
If MRSA* isolated >50% in
ICU
Consider adding vancomycin.
Pathogen
Anaerobic
Risk Factor
Observed
aspiration
Antibiotic
Clindamycin, metronidazole, or Beta-lactam/beta-lactamase
inhibitor
Abdominal
surgery
Putrid discharge
Staphylococcus
aureus
Coma
Vancomycin
Head injury
Diabetes
Renal failure
MRSA*
Outbreaks
Vancomycin
Legionella species
Corticosteroid use
Erythromycin
Outbreaks
Pathogen
Risk Factor
Antibiotic
Pseudomonas aeruginosa
Prolonged ICU stay
As in severe hospital
acquired pneumonia (see
Table: "Antibiotics for
patients with no risk
factors" above)
Antibiotic exposure
Chronic lung disease
AIDS