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Mucormycosis (previously called zygomycosiss ) is a life-threatening fungal infection that occurs in immunocompromised patients. These infections are becoming increasingly common, yet survival remains very poor. Fungi of the order Mucorales are causes of mucormycosis, a life-threatening fungal infection almost uniformly affecting immunocompromised hosts in either developing or industrialized countries.
Mucor is mainly found in soil, digestive systems, plants surfaces and rotting vegetable matter. It is a microbial genus of molds that can cause infection to human beings. Upon inhaling fungal spores from the environment, one can develop infections in the lungs, sinuses, eyes as well as face. The infection can be developed through cutaneous routes, the fungi can enter the skin via cuts, scrapes, puncture wounds, or other forms of trauma to the skin. In the hospitals this can happen through catheters and other invasive procedures. It is noted that this infection is becoming more of a nosocomial infection. Mucormycosis does not spread from person to person thus not contagious. People suffering from diabetes, extensive burns, and immunosuppression symptoms associated with AIDS and other afflictions, organ transplants, or those who are intravenous drug users, appear to be most susceptible to Mucor infections.
The genus Mucor contains several species. The most common ones are Mucor amphibiorum, M. circinelloides, M. hiemalis, M. indicus, M. racemosus, and M. ramosissimus. To cause disease, the agents of mucormycosis must scavenge from the host sufficient iron for growth, must evade host phagocytic defense mechanisms. Mucor after gaining entrance to host, invades the alveoli. Then the spores begins to penetration into spaces between the cells before spreading to adjacent cells. With fungi in the lungs, the patient’s body reacts by activating its immune system resulting in an increase in leucocytes. The leakage of fluids from blood vessels to alveoli results in pneumonia.
With pneumonia we are looking at impaired airway and gas exchange issues, so patient will benefit from oxygen therapy. Keep the head of the bed elevated for better oxygenation and aspiration precaution. Frequent monitoring of vital signs and oxygen saturation should be initiated. Assess patient for pain and discomfort and treat as ordered. Initiate use of incentive spirometer as soon as possible to aid in the recovery of the lungs.
The abnormal lab values include WBC- 15,200/mm3-indicating infection, PH of 7.50, PaO2 of 59mg, HCO3 of 29, and PaCO2 of 25 -indicated the body is alkaline but partially compensated – through hyperventilation and Lymphocytes 10%- the patient is immunocompromised.
It is now clear that iron metabolism plays a central role in regulating mucormycosis infections and that deferoxamine predisposes patients to mucormycosis by inappropriately supplying the fungus with iron. These findings raise the possibility that iron chelator therapy may be useful to treat the infection as long as the chelator does not inappropriately supply the fungus with iron. Recent data support the concept that high-dose liposomal amphotericin is the preferred monotherapy for mucormycosis. These options include combination therapy using lipid-based amphotericin with an echinocandin or with an azole (largely itraconazole or posaconazole) or with all three. The underlying principles of therapy for this disease remain rapid diagnosis, reversal of underlying predisposition, and urgent surgical debridement.
Lipid formulations of Amphotericin B deoxycholate (LAmB) are significantly less nephrotoxic and can safely be administered at higher doses for a longer period (Spellberg, 2010).
Amphotericin B deoxycholate (AmB) has been effective in treating mucormycosis and is more affordable than other drugs. Dosage is 1-1.5 mg/kg/d with a total of 2.5-3 g for the whole therapy.
Posaconazole 400 mg BID (total 800 mg/d). This has been effective in those patients who fail treatment with Amphotericin B or used conjunctively after the initial Amphotericin B treatment.
It is also important to address the predisposing condition of the susceptible patient. Those with diabetic ketoacidosis need insulin, hydration, and sodium bicarbonate to reverse the condition. Colony stimulating factors for those with neutropenia. Weaning off immunosuppressive drugs can
help boost treatment.