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Hello i need a Good and Positive Comment related with this argument .A paragraph  with no more  100 words.

Chinyere Ojiyi 

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. 


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