Yes, it should be ok.  Lysozyme helps break down G+ cell walls because it works on peptidoglycan.  Fungi have chitin in their cell walls not peptidoglycan.

Lysozymes enzymes is breaking  glycodide bound between N-acetylglucosamine and N-acetylmuramic acid in peptidoglycan. This  bound not found in fungi wall. This wall have chitin , protein and fat.

Lysozyme is specific enzyme. 

Yes, Lysozyme will be the ideal choice. fungal cell wall is not affected by lysozyme.

You could treat both  organisms with antibiotic Penicillin, where it will beak down Gram -positive bacteria cell wall, leaving fungi cell wall safe

why dont you try KOH

Thank you all for confirming that lysozyme works specifically for bacteria without hurting fungi. 

Dear Yehia,

Lysozyme is the only  thing I know that might work. You suggested the atibiotic penicilllin. Just confirm with you that penicillin will work the same way as lysozyme. What is the difference between lysozyme and penicillin toward breaking down bacteria cell wall?

Thanks,

Dear Ramana,

Could you explain more on using KOH? Will KOH break down bacteria cell wall without hurting fungi cell wall? What is the mechanism? I only know bacteria prefer acid conditions. 

Thanks,

Dear Aiqin 

The lysozyme is specific in break dawn for G+ wall. Penicillin was added to media culture for inhibition G- wall growth.

KOH and NaOH  are use increase pH media to 11-12 and low pH to 1-2. The method is not specific and to lead break dawn for fungi wall 

Deal all,

Alaa mentioned that Penicillin breaks down G negative bacteria cell wall while Yehia said it breaks G positive cell wall. I am confused. The major bacteria we used are G positive bacteria.  Will Penicillin work for G positive bacteria?

One more question, the break-down of bacteria by lysozyme will affect bacteria protein or not?

Thanks

Dear Aiqin

Please read down I transfer from  en.wikipedia.org/?title=Penicillin 

Bacteria constantly remodel their peptidoglycan cell walls, simultaneously building and breaking down portions of the cell wall as they grow and divide.β-Lactam antibiotics inhibit the formation of peptidoglycan cross-links in the bacterial cell wall; this is achieved through binding of the four-membered β-lactam ring of penicillin to the enzyme DD-transpeptidase. As a consequence, DD-transpeptidase cannot catalyze formation of these cross-links, and an imbalance between cell wall production and degradation develops, causing the cell to rapidly die.

The enzymes that hydrolyze the peptidoglycan cross-links continue to function, even while those that form such cross-links do not. This weakens the cell wall of the bacterium, and osmotic pressure becomes increasingly uncompensated—eventually causing cell death (cytolysis). In addition, the build-up of peptidoglycan precursors triggers the activation of bacterial cell wall hydrolases and autolysins, which further digest the cell wall's peptidoglycans. The small size of the penicillins increases their potency, by allowing them to penetrate the entire depth of the cell wall. This is in contrast to the glycopeptide antibiotics vancomycin and teicoplanin, which are both much larger than the penicillins.[18]

Gram-positive bacteria are called protoplasts when they lose their cell walls. Gram-negative bacteria do not lose their cell walls completely and are called spheroplasts after treatment with penicillin.

Penicillin shows a synergistic effect with aminoglycosides, since the inhibition of peptidoglycan synthesis allows aminoglycosides to penetrate the bacterial cell wall more easily, allowing their disruption of bacterial protein synthesis within the cell. This results in a lowered MBC for susceptible organisms.

Penicillins, like other β-lactam antibiotics, block not only the division of bacteria, including cyanobacteria, but also the division of cyanelles, thephotosynthetic organelles of the glaucophytes, and the division of chloroplasts of bryophytes. In contrast, they have no effect on the plastids of the highly developed vascular plants. This supports the endosymbiotic theory of the evolution of plastid division in land plants.[19]

The chemical structure of penicillin is triggered with a very precise, pH-dependent directed mechanism, effected by a unique spatial assembly of molecular components, which can activate by protonation. It can travel through bodily fluids, targeting and inactivating enzymes responsible for cell-wall synthesis in gram-positive bacteria, meanwhile avoiding the surrounding non-targets. Penicillin can protect itself from spontaneous hydrolysis in the body in its anionic form, while storing its potential as a strong acylating agent, activated only upon approach to the target transpeptidase enzyme and protonated in the active centre. This targeted protonation neutralizes the carboxylic acid moiety, which is weakening of the β-lactam ring N–C(=O) bond, resulting in a self-activation. Specific structural requirements are equated to constructing the perfect mouse trap for catching targeted prey.[20]

• Dear Aiqin: Read the following_

Antimicrobial Spectrum of Penicillins

Penicillins have a bacteriocidal effect on Gram-positive bacteria. In Gram-positive cells, peptidoglycan makes up as much as 90% of the thick, compact cell wall, and is the outermost layer.

Penicillins are not effective against Gram-negative bacteria, which have cell walls in which peptidoglycan is not the outermost layer, but that lies between the plasma membrane and a lipopolysaccharide (LPS) outer membrane. Penicillin cannot access the peptidoglycan of Gram-negative cells.

• Please, look into this link:
• http://www.scienceprofonline.org/microbiology/mode-of-action-of-penicillin-antibiotic.html

why dont you try different concentrations of KOH (10%, 20%, 40%), we see that at this concentrations fungal morphology is not disturbed.