Alongside such rapid proliferation is a corresponding mass-production of exotoxin that causes severe damage to local tissue in the host. One such exotoxin is alpha toxin, which is produced by C. perfringens and is the key virulence factor in its pathogenesis.Massive infection, gross injury, and depletion of the hosts immune capability result in system-wide sepsis. This is partly due to the burden on the immune system, its corresponding release of inflammatory cytokines, and the distribution of bacterial toxins. Massive infection is likely to result in death from a combination of system-wide septic shock and the unintentionally damaging effects of the immune response. In animals, disability and distress caused by all of these factors markedly increase the chance of predation. Diagnosis
Various diagnostic methods can be employed in the diagnosis of Gas gangrene. Due to low incidence of myonecrosis it is an easy-to-overlook diagnosis. As bacterial infections mostly exhibit the same symptoms, early diagnosis of gas gangrene rarely occurs. The ambiguous symptoms only contribute to a poorer prognosis. Diagnostic methods include:
Biopsy of affected tissue
Cultures of fluids from inflicted area
Magnetic resonance imaging to visualize necrotized subcutaneous tissues
X-rays for air pockets in affected tissues
Microscopy identification of strain of bacteria sampled from fluids of inflicted area
Gram stain

Treatment
Treatment is usually debridement and excision, with amputation necessary in many cases. Water-soluble antibiotics (such as penicillin) alone are not effective because they do not penetrate ischaemic muscles sufficiently to be effective. Penicillin is effective against C. perfringens.
Xerophthalmia from hypovitaminosis A is specifically due to lack of the hormone-like vitamin A metabolite retinoic acid, since (along with certain growth-stunting effects) the condition can be reversed in vitamin A deficient rats by retinoic acid supplementation (however the retinal damage continues). Since retinoic acid cannot be reduced to retinal or retinol, these effects on the cornea must be specific to retinoic acid. This is in keeping with retinoic acids known requirement for good health in epithelial cells, such as those in the cornea. Cause
The condition is not congenital and develops over the course of a few months as the lacrimal glands fail to produce tears. Other conditions involved in the progression already stated include the appearance of Bitots spots, which are clumps of keratin debris that build up inside the conjunctiva and night blindness, which precedes corneal ulceration and total blindness. Classification
World Health Organization classified xerophthalmia into following stages:
XN-Night blindness
X1A-Conjunctival xerosis
X1B-Bitot spots
X2-Corneal xerosis
X3A-Corneal ulceration/keratomalacia, involving less than one-third of the cornea
X3B-Corneal ulceration/keratomalacia, involving more than one-third of the cornea
XS-Corneal scar due to xerophthalmia
XF-Xerophthalmic fundus

Prevention
Prophylaxis consists of periodic administration of Vitamin A supplements.