INTRODUCTION:

R.D. Baker, an American physician, introduced the name Mucormycosis. Zygomycosis is another name for this disorder. Members of the Mucorales and zygomycotic species commonly refer to it as an insidious mycosis¹. The cellular structural arrangement of the fungus is unique, and it contains a higher content of carbohydrate as a polymer of N-acetyl glucosamine than peptidoglycan in most bacteria. Rhizopus, Abydia and Cunningham Ella are the main mucus species. Uncontrolled diabetes mellitus is the focal point for accelerating myocorrhosis^1,2.

Zygomycosis and Mucormycosis occur in the soil and their aerobic ovulation causes infection. The main symptoms here are thrombosis and tissue necrosis in mycosis. Mycorrhizae is a rare but severe invasive fungal infection, described primarily in immune diseases³. Mucormycosis has the feature of invading the angiogenesis causing thrombosis and tissue necrosis. Diagnostic and treatment approaches, including the early involvement of a multidisciplinary medical, surgical, radiological, and laboratory-based team, need needed to increase survival rates. PCR-based procedures can detect and accurately identify Mucoral fungi in clinical samples. Improved survival is generally associated with early, multi-disciplinary treatment modalities involving prior diag.nosis and non-invasive surgery^1,4. Mucorals are not vesicular organisms and grow on a temperature background (25⁰C - 5⁰C); The optimum temperature for the growth of clinically important species of Mucorales is 28⁰-30⁰C the isolation obtained from clinical specimens will also increase to 37⁰C. In the microbiology laboratory the organisms grow and proliferate within 2–5 days after incubation^1,2.

History:

Mucormycosis grew increasingly common in immunocompromised people in the 1980s and 1990s. According the incidence rates, a study conducted in France found that amplification occurs at a rate of 7.4 percent every year⁶. Mucorales infection has been known to occur all over the world, with the possibility of seasonal change. The condition was initially documented in 1876 by Fürbinger in Germany, who described a patient who died of cancer and had a hemorrhagic infarct in the right lung with fungal hyphae and a few sporangia ⁶. Arnold Paltauf recorded the first case of disseminated Mucormycosis in 1885, calling it "Mycosis mucorina." Roden et al. published the first comprehensive evaluation of the literature in 2005.

Types:

The agents of Mucormycosis are classified in the order of mucosa. The mycelium of this fungus is composed of non-septate, coenocytic hyphae, which have morphological features exhibited by them in the tissues of the infected host. Pathogenic members of this fungal order reproduce toxins in the sac or sporangium, or by sporangiospores born of candidiasis. The appearance of sporangium and spore-bearing structures are the main basis for family differences in the order of Mucorales.

Infection types:

Infection with human corpuscles occurs in two forms.

1 Superficial and Visceral and

2. Localized and transmitted.

Superficial form occurs in the outer ear, nails, skin. Visceral forms manifest as lung, gastrointestinal, and cerebral types. They are broadly classified as,

Table 1 Classification of Mucormycosis 8,9:

Sr. No	Types	Route of transmission
1	Rhinocerebral (sinus and brain) Mucormycosis	Inhalation of spores into the of spores into the paranasal sinuses and the invasion of blood vessels in the tissue
2	Pulmonary (lung) Mucormycosis	Inhalation of infectious material
3	Gastrointestinal Mucormycosis	The ingestion of contaminated food/ herbal medicine
4	Cutaneous (skin) Mucormycosis	Skin infection by direct inoculation and in secondary form, by dissemination from other locations.
5	Disseminated Mucormycosis	Blood stream

Etiopathogenesis:

The mucous membrane penetrates deep tissues, swallowing or inhaling spores and injecting them into the skin. Once the spores enter the lungs or skin tissue, the first line of defense of a healthy host can destroy them using oxidative metabolites and cationic peptides ¹⁰. Fungal spores enter the human body through inhalation, ingestion, or direct infection. The causative agents of Mucormycosis differ depending on the geographic region. The sinuses (39%), lungs (24%) and skin (19%) were most often affected. Pulmonary mycosis is related to hematologic malignancies and neutropenia, and diabetes mellitus is related to sinusitis and non-encephalopathy, whereas cutaneous Mucormycosis is frequently caused by trauma¹¹. Calcineurin is essential in the pathogenicity of opportunistic fungus, such as primary cutaneous Mucoromycosis¹². It progresses very slowly, in contrast to the classic manifestation associated with treatment of Mucormycosis.

Inhalation causes pulmonary and non-cerebral infections, while taking pills or food and taking tongue sedatives causes mucormycosis of the gastrointestinal tract. In particular, in the case of the central nervous system, the mortality rate often exceeds 80%. In contrast, lower mortality was observed with local infections of the nasal sinuses or skin¹³.

Risk factor:

Serious skin lesions such as organ neutropenia, intravenous drug use, malnutrition, stem cell or solid organ transplants, burns, and surgical stitches. Neutropenic patients and patients with elevated serum iron levels are also at increased risk, with decreased immunity being a major risk factor¹¹. Immunosuppressants further increase the risk of fungal infections. Risk factors include uncontrolled diabetes mellitus, especially ketoacidosis, steroid use, age, neutropenia; Voriconazole, especially for the prevention of blood cancer, AIDS, renal failure, organ or stem cell transplantation, iron overload, skin trauma, broad-spectrum antibiotics, intravenous drug use, aspergillosis and malnutrition^7,11 Mucormycosis can also occur in patients without overt immunodeficiency. These conditions can be associated with burns, trauma and / or iatrogenic factors. Chronic corticosteroids and other immunosuppressants.

Predisposing factors:

Mucormycosis is associated with exposure to high levels of airborne fungal contamination from various health-related procedures and devices, such as construction work, contaminated air filters or contaminated wound dressings, transdermal nitrate patches, intravenous catheters, tongue sedatives, and even pills allopurinol. The disease is also associated with high mortality. Expected frequencies range from 0.4% ma to 16.0% depending on the type of SOT (Sacro Occipital Technique) from 0.2% to 1.2% for kidney transplant recipients and from 0% to 1.6% for liver transplant recipients, 0% - 0.6% heart transplant recipients, 0% -1.5% lung recipients. Other illnesses associated with mucositis include intravenous drug use, AIDS, Kidney failure, Liver disease, Chronic alcoholism, and malnutrition.

Causative agent:

The order Mucorales consists of 55 genera and 261 species, 38 of which are associated with human infection¹⁴. Their taxon has changed significantly in recent years as a result of molecular phylogenetic studies, and, of course, some taxa have been renamed. The current nomenclature of this taxon is shown in Table 2¹¹.

Table 2 Current nomenclature of medically important mucoralean species according to updated taxonomy¹⁵

Current Species Names	Previous Names/Synonyms
Lichtheimia corymbifera	Absidia corymbifera,Mycocladus corymbifer
Lichtheimia ornata	Absidi aornata
Lichtheimia ramosa	Absidi aramosa, Mycocladusramosus
Mucor ardhlaengiktus	Mucor ellipsoideus, Mucor circinelloides f.circinelloides
Mucor circinelloides	Rhizomucor regularior,Rhizomucor variabilisvar.regularior
Mucor griseocyanus	Mucor circinelloides f.griseocyanus
Mucor irregularis	Rhizomucor variabilis
Mucor janssenii	Mucor circinelloides f.janssenii
Mucor lusitanicus	Mucor circinelloides f. lusitanicus
Rhizopusarrhizus (incl.var.delemar)	Rhizopusoryzae

Mucormycosis- Post Covid Complications:

SARS-CoV-2 (Severe acute respiratory syndrome coronavirus 2) is a single-stranded, positive-sense RNA virus. The spike (S), envelope (E), membrane (M), and nucleocapsid (N) structural proteins make up the SARS-CoV-2 virion, which has a diameter of 50 - 200nm. The S protein enables the virus to bind to the cell membrane of the host. S proteins have been discovered to target the angiotensin-converting enzyme 2 (ACE2) receptors on host cells¹⁶.

The main pathogenesis of COVID-19 infection was severe pneumonia, ARDS (Acute respiratory distress syndrome), RNAaemia, combined with the incidence of ground-glass opacities, and acute cardiac injury¹⁷.

The major symptoms of COVID-19 are breathlessness, dry cough, and fever with body weakness, but 50% of patients might be asymptomatic or present mild symptoms, although they would still be highly infectious. In some cases, loss of smell and other severe effects such as blood clot formation have been reported ^18,19.

In the context of COVID-19, India has seen an increasing number of incidents. Even from standard antifungal treatment, fatality rates have been shown to be extremely high. According to statistics, about 12,000 cases of infection have been reported, with many more unreported. There were 11,717 confirmed cases of mucormycosis in India on May 26, 2021. The Centers for Disease Control and Prevention (CDC) reported a 54 percent overall fatality rate before the pandemic Trusted Source²⁰.

COVID-1950 is diagnosed in patients who meet clinical case definition and are epidemiologically linked to a history of travel or who have come into contact with a reverse transcription (RT)-PCR confirmed case or a patient who is under investigation for SARS-COV-2 during that time. Expectorated sputum, BAL fluid, end tracheal aspirate, and tissue swabs taken with Dacron swabs are all preferable clinical samples for establishing laboratory evidence of a reported occurrence²¹.

Dexamethasone could save the lives of crucial SARS-CoV-2 patients, according to preliminary clinical findings published by the World Health Organization and the United Kingdom. On June 16, 2020, the FDA approved dexamethasone for the treatment of coronavirus. Treatment reduced fatalities by one-third in patients who had ventilators, but only by one-fifth in patients who merely needed oxygen²².

The majority of the cases documented are related to the inappropriate use of corticosteroids in COVID-19 patients, who frequently also have uncontrolled diabetes. It's worth noting that corticosteroids are life-saving, and millions of people infected with the SARS-COV-2 virus in the Western world (the United States, the United Kingdom, and Europe) have been treated with them. When the treatment methods are practically the same, India reported 70% mucormycosis compared to the rest of the world. In India, uncontrolled diabetes is common, and the majority of patients do not have their blood sugar levels checked on a regular basis. Furthermore, several of these individuals were prescribed far more dexamethasone than the recommended amount of 6.0 mg/day for 5–10 days²³. Because some of the patients who acquired diabetes during their COVID-19 illness had never had diabetes before, it's possible that it was caused by SARS-affinity CoV-2's for the ACE2 receptor causing damage to pancreatic beta cells. Diabetes mellitus (73.5%), ma-lignancy (9.0%), and organ transplantation are among the main risk factors for mucormycosis²⁴.

Diabetes as Risk Factor:

According to the World Health Organization (WHO). The most prevalent type of diabetes among adults with diabetes is type II diabetes, that is uncontrolled. In diabetic patients, Mucormycosis develops as a destructive and potentially fatal condition due to the increased availability of micronutrients and a decrease in the body's defense mechanisms. All types of mucositis occur in diabetes mellitus, especially ketoacidosis. Neutrophils play an important role in protecting the host from mucous membranes. Diabetic ketoacidosis accelerates fungal invasion. An acidic environment reduces binding to transferrin, producing more free iron, and low levels of dialysis inhibitors in diabetic patients create favorable conditions for fungal growth.

Table 3 Risk factors in diabetics

Factors for increased risk in diabetics

· Beta hydroxybutyrate leads to dissociation of iron from its sequestering proteins. Free iron

· increases fungal survival and virulence

· Upregulation

· of GRP78: Enhances tissue penetration

· Hyperglycation of iron sequestration proteins

· Reduced phagocytosis due to impaired gluthathione pathways

· Expression of Ketone reductase that helps it thrive in acidic environment

Diagnosis:

Early diagnosis of Mucormycosis is very important because it can reduce the need or frequency, disability, and pain of surgical resection⁵. The accessibility of imaging techniques, trained staff, and mycological and histological exams all play a role in Mucormycosis diagnosis. Patients with suspected mucormycosis should be moved as soon as possible to the most advanced medical facility²⁵. This clinical approach to diagnosis has low sensitivity and specificity. In India, the main cause of this disease is Rhizopus species present in air, that inoculates organisms in the air or directly onto the skin mucosa or gastrointestinal tract²⁶.

Mucormycosis diagnosis involves a careful examination of clinical manifestations, magnetic resonance imaging modalities, early use of computed tomography (CT), expert evaluation of cytological and histological provision, best application of clinical microbiological technique, and molecular detection²⁷. For patients with diabetes mellitus and newly diagnosed facial pain, sinusitis, protrusion, ophthalmoplegia, melanoma, or both, a cranial CT or MRI scan is recommended to check for sinusitis.

Diagnosis is usually based on clinical suspicion and histopathological examination. Clinical diagnosis of mycorrhiza in the lungs in patients with nonspecific symptoms such as cough, shortness of breath, chest pain and fever is difficult. PAS (Periodic acid–Schiff) stain, direct analysis, calcofluoride, histopathological examination, silver staining with mesalamine, molecular techniques and fluorescence in situ hybridization are other laboratory methods for Mucor detection. Microbiological diagnosis is mainly made by mucosal isolation or direct positive staining of clinical specimens ²⁵.

Molecular Methods:

Molecular methods have been developed as a useful tool to confirm infection and identify stress participants. The ITS (internal transcribed spacer) region is the most widely sequenced DNA region for fungi in general. ITS sequencing is a valid technique that has shown to be highly helpful for molecular systems at the species belonging and in molecular species. It is indicated for a first tool for detecting Mucoralis species. PCR-based techniques such as Nested PCR, Real-Time PCR (QPCR), Nested PCR, RFLP, PCR and Electrospray Ionization Mass Spectrometry (PCR/ESI-.MS) and PCR/high-resolution melt analysis have been established for tissue investigation (HRMA). These techniques have been tried and tested, and they function efficiently on fresh or deep-frozen samples than on paraffin-embedded tissues.

Most molecular tests target 18S ribosomal RNA genes, but other targets have also been detected. Fresh ingredients are preferred over paraffin-embedded tissues because formalin damages DNA.

Serology:

Antigen markers for screening mucorales as galactomannan (GM) for aspergil-lus are not commercially available. In haematology patients or patients with persistent chest CT imaging, however, GM testing in blood pressure and BAL can be used to lower the risk of mucosal mycosis²⁷. In addition, pan fungal-D-glucan testing does not detect antigenic components of the mucoralus²⁶.

Radiographic Features:

A CT scan of the head reveals dense mucous membranes or cloudy sinuses, densely crowded extra ocular muscles, increased compactness of the orbital vertices, proptosis, and inflammation of the optic nerve. The results of CT scans and magnetic resonance imaging (MRI) scans have been reported recently²⁶. CT scans of the head show evidence of sinus involvement which is related to sinus opioids' other chances of infection may be less. MRI scans may also reveal abnormalities in the structures involved. The involvement of the sinuses may be noticed by the presence of mucosal thickening or secretions.

Histopathology:

Histopathology is a very important diagnostic tool as it is necessary to determine the presence of fungi as pathogens in culture-contaminated samples and to determine if there is an invasion of blood vessels. It can also indicate coinfection with other fungi. The details of the events that trigger network prophylaxis on the network are largely unknown. Typical fungal mycelium detection of mucous hyphae in tissue biopsies or in bronchoalveolar lavage (BAL) fluid from patients with pulmonary mycosis. On examination, the affected tissue shows extensive necrosis with many pale branches and wide flat septal hyphae with right or blunt branches²⁷.

Routine hematoxylin and eosin (H and E) stains show only on the cell wall. The stains that help highlight the fungal wall are Grocot Methanamine-Silver (GMS) and the PAS stain.

Symptoms:

Mucormycosis can impact the nose, orbit, sinuses, pulmonary, CNS, gastro-intestinal tract (GIT), skin, jaw bones, joints, heart, kidney, and pulmonary trunk (invasive type). (Table-4).

Treatment approaches:

The ability to effectively treat mucositis depends on the surgical technique and the availability of antifungal drugs. Immunosuppression is a key component of modern fungal therapies. The currently available monotherapy specifically shows high mortality rates with hematology patients and is therefore proposed to choose “combination therapy” for mucormycosis. In the case of soft tissues, surgical treatment of cerebral proliferation, local lung lesions and rhino-orbito type should be consider.

Surgical:

Extensive surgical debridement is probably the most important option for the treatment of patients with mucositis and this option should be discussed immediately. The goal of surgery is to remove all the deformed tissue²⁶. Debreeding may need to be repeated daily for several days. The type of surgical procedure is determined by the extent of the patient's infection^7.

Antifungal therapy:

Newer generation antifungal treatments such as amphotericin B, ketoconazole, itraconazole, and voriconazole. Amphotericin B (AmB), result in the lowest minimum inhibitory concentration (MIC) against mucor species.

Voriconazole results in higher MIC. Amphotericin B is the most effective drug. There are several formulations of amphotericin B available, including liposomal and lipid-based amphotericin, the colloidal diffusion of amphotericin for most common fungal infections^3,7. Antifungal treatments include liposomal AmB (5-10mg /kg), AmB lipid complex, AmB colloidal diffusion, second-tier treatment with caspofungin and lipid AmB, a mixture of lipid AmB and posaconazole. Breakthrough invasive fungal infections persist when new azoles, posaconazole, and isavuconazole are introduced, despite their anti-mucoral activity¹⁷.

First line antifungal monotherapy:

Daily liposomal amphotericin B with 5-10mg/kg is strongly supported in all samples of first-line treatment organ involvement¹³. Patients without amphotericin B lipid complex CNS are recommended 5mg/kg daily with moderate potency. For the first-line therapy of mucormycosis, isavuconazole with a moderate potency is indicated. For first-line treatment, this group highly recommends the use of pozoconazole oral suspension and moderately recommends the use of pozoconazole delayed release tablets and infusions.

First line antifungal combination therapy:

The benefits of double and triple antifungal combinations in patients with hematologic disorders were not proven. Multiple mould species combined therapy either by posconazole or voriconazole is indicated in traumatised patients, especially in blast injuries. Antifungal salvage treatment.

There are usually two drug-related causes for treatment failure, refractory mucormycosis or toxicity of first-regiments - that is, intolerance to a drug. For amphotericin B formulations, especially renal toxicity may be a limiting factor. Toxicity is expected due to previous antifungal or pre-existing organ damage. Isavuconazole preventive treatment is successful in both clinical scenarios, refractory diseases, and intolerance or toxicity. Pozaconazole treatment with oral suspension was cured in two non-randomized clinical trials. Treatment Pozaconazole is strongly supported for delayed release tablets or infusion rescue treatment and when available⁷.

Treatment duration for mucormycosis:

The duration of therapy required for the treatment of mucormycosis is not known. In general, therapy is given for weeks to months. If the immune defect is removed - e.g. If diabetes is controlled, neutropenia is definitely resolved, immunosuppression can be tempered or stopped, therapy can be continued until signs and symptoms of infection are resolved, and significant radiographic improvement occurs. The median duration of isavuconazole first-line or rescue treatment was 84 days intravenously or orally or both⁴. According to several studies, Pozaconazole oral suspension the duration of treatment ranged from 1 week to 3 years, i.e., about 6 months. When switching to oral treatment, the use of isavuconazole or pozaconazole delayed release tablets is strongly supported. Surgical debridement should be performed whenever possible in parallel with antifungal treatment²⁸. Isvuconazole or pozaconazole may be given as maintenance therapy. Therapeutic modalities of patients taking amphotericin B to enhance antifungal activity include the inclusion of rifampin or tetracycline in the unpleasant treatment of mucormycosis.

Prevention:

Cleaning and replacement of humidifier bottles (for individuals who use oxygen concentrators). The humidifier bottle should be disinfected with normal saline and replenished on a regular basis. Masks should be disinfected on a regular basis and should not be worn for more than a week. Steroid users should keep an eye on their blood sugar levels. Mortified oxygen should be used during COVID-19 therapy ²⁵.

CONCLUSION:

Mucormycosis is a disease that is rare but has a significant burden on patients with immune compromise. Despite presence of newly developed drugs, curing mucosal infection is still a challenge, but given its high mortality rate, early and prompt diagnosis, recovery from potential factors, early surgical intervention from this devastating disease The only hope for improvement is dehydration and therapeutic drugs.

Lack of selective methods for diagnosis, culture and treatment of fungal infections leads to necrotic and inflammatory effects of mucormycosis. More, much-needed, quicker approaches, such as serology-based, metabolism-based breathing tests, are now being developed and will hopefully be studied in the near future.

CONFLICT OF INTEREST:

The authors have no conflicts of interest regarding this investigation.

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Received on 01.06.2022 Modified on 24.07.2022

Asian J. Res. Pharm. Sci. 2022; 12(4):297-303.

DOI: 10.52711/2231-5659.2022.00051

Symptoms of Mucormycosis