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CASE 4:

A 60 year old male who is 4 months post orthotopic heart transplant for ischemic cardiomyopathy present with a 2 week history of increasing pain, swelling and tenderness in his right thigh. The patient also has a history of fever to 101° over the last 2 days. Meds: Cyclosporin, prednisone and azathioprine.

Physical examination: T. 38.0°C, BP 140/80, R-14, HR 80, No acute distress. Lungs: Clear, CV - S. and S2 NL no S3/ S4 Abd: soft, non-tender, no organomegaly. Ext: (R) thigh swollen red tender fluctuant 3cm x 3cm mass, some surrounding cellulitis Neuro: WNL

Laboratory: CXR: 2cm nodules in (R) upper lung, WBC 6.1, 88p, 8 bands, 2 L, 2 mono Aspirate of the lesion shows acute inflammation and gram-positive irregularly stained or beaded, branching filamentous organisms, modified Ziehl-Nielsen stain of the aspirate disclose acid fast organisms seen with the same morphology.

QUESTIONS:

1. Create a problem list from the history.

s/p Heart transplantation
On Immunosuppressive therapy
Painful swollen right leg
Febrile acute illness

2. Identify and explain the significance of each pertinent physical finding.

Fever
Cellulitis with a fluctuating tender mass in thigh

3.Review the lab data and explain the findings.

Solitary pulmonary lung nodule in CXR
Signs of bacterial infection in CBC
gram-positive irregularly stained or beaded, branching filamentous organisms, modified Ziehl-Nielsen stain of the aspirate disclose acid fast organisms seen with the same morphology.

4. What is diagnosis based on History, physical and lab data.

Nocardial infection

5. Describe succinctly, the disease each case represents

Increasing incidence of infection with Nocardia
Follows increase in organ transplantation and the attendant immunosuppressive therapy

6. Describe the offending organism, its morphological, cultural characteristics and their normal habitat.

Nocardia asteroides, Nocardia brasiliensis.

Branching filamentous
gram-positive bacterium
Weakly acid-fact.
Long, delicate not beaded.
Aerobic bacterium.
Does not form spores

Found worldwide in soil and decaying organic material

7. How do these organisms gain access to humans?

Nocardia infects humans through the respiratory tract.
Nocardia may also be introduced through the skin.
Nocardia will disseminate via the blood or lymphatic channels.

8. Who are susceptible hosts?

Increased incidence in people with deficient cell mediated immunity
Immunosuppressive therapy for transplantation.
Approx. 1,000 cases of nocardiosis diagnosed annually in the U.S.

33 - 50% immunocompromised Transplant (45%), long term use of steroids Lymphoma / leukemia, HIV, post splenectomy

9. How do they invade and spread in humans?

Opportunistic infection

10. What defenses humans have against these organisms?

Immune T-cells are important in clearing Nocardia from the lung and preventing dissemination.
Inflammation is also neutrophilic but infections progress unless antimicrobial agents are given or cell mediated immunity takes over.

11. How do these organisms able to overcome human defenses?

Opportunistic infection.
They can thrive only if there is defect in cell mediated response

12. What is the end result of this battle between organisms and humans?

Subacute or chronic abscess

13. How do you diagnose this infection?

Transthoracic percutaneous fine needle aspirate (Under CT guidance) or bronchoscopy.
Skin biopsy or aspiration of lesion

14. What are other clinical infections with these organisms?

Lungs most common site of involvement -- 70-80% of cases Pulmonary nocardiosis -- subacute (may have acute onset in immunocompromised hosts) cough, sputum, fever , anorexia , wt. loss CXR >> variable infiltrates , nodules, cavities

However, dissemination to nearly every organ has been reported i.e., kidney, bone, muscle, peritonitis, endocarditis
Extrapulmonary dissemination typically presents as subacute or chronic abscess

The CNS is infected in about 1/3 of all cases. Nocardial Brain Abscess

2.5 times more common in males than females
Usually one or more supratentorial brain abscesses, often multiloculated with satellite extensions
Rupture into ventricles can lead to acute deterioration -- meningitis Common presenting features -- headaches, seizures, confusion and focal neurologic findings

15. What will be your therapeutic strategy?

Trimethoprim-sulfamethoxazole
Imipenem / Amikacin
Cefotaxime / Amikacin I.V. for at least 6 wks.
Immunocompromised ---- 1 yr. of oral Antibiotics
(following I.V. Tx)
Brain abscess
- Stereotactic aspiration / decompression of brain abscesses
- Craniotomy to excise the entire abscess and wall

16. How can you prevent it from spreading to others? Prevent its occurrence?

It is not a contagious infection.
It is an opportunistic infection
No preventive measures can be taken