• Demonstration of a normal pH, the absence of any other pathogen, presence of yeast and/or pseudohyphae, establish the diagnosis of Candida vaginitis.
•  The addition of 10-20% KOH is helpful in lysing other epithelial cells and aiding in visualizing yeasts or pseudohyphae; in 30-50% of infected women direct microscopic examination fails to demonstrate Candida and a presumptive diagnosis must be made. 
• Most routine media will grow Candida. The formation of germ tubes, on incubation for 90 min in serum allows a presumptive identification of albicans. 
• Further biochemical tests are required to differentiate the non albicans Candida species.

• "Yeast" forms are budding blastoconidia and "Pseudohyphae" which are elongated processes arising from blastoconidia and possess different chemical and enzymatic properties. 

• The pseudohyphae are seen in association with invasive forms of tissue infection.
  
  

What is the likely diagnosis? How is the diagnosis established? 

• Vulvovaginal candidiasis

Other agents causing vaginitis are 

• Trichomonas vaginalis , a protozoan that produces a foamy, malodorous yellow-green discharge, 

• Bacterial vaginosis, caused by anaerobic bacteria such as Bacteroides, Mobiluncus, and gram negative bacteria such as Gardnerella vaginilis. A white discharge with fishy odor and clue cells on microscopic examination help establish this diagnosis. 

• Neisseria gonorrhea, which produces a vaginal discharge in conjunction with a cervicitis.
  
  

What factors facilitate causation of disease by this organism? Which of these was most important in our patient? 

• Colonization is aided by the ability of Candida to adhere to mucosal surfaces. Overgrowth of Candida may be facilitated by high estrogen levels particularly in pregnancy. 
• Normally ,other flora (bacteria) resident on mucosal surfaces prevent uncontrolled proliferation by Candida, high population density and subsequent disease are facilitated by suppression of normal flora by antibacterial agents, such as ampicillin treatment in our patient.
•  Pseudohyphae bind to components of the extracellular matrix; proteinases help in invasion and adherence. 
• High sugars in diabetics enhance production of surface adherence proteins such as mannoproteins of the outer fibrillar surface of Candida.
•  Disruptions of skin and mucosal surfaces expose components of the ECM to which Candida can bind. 
• Corticosteroids and depressed T cell immunity also predispose to local and invasive disease.
  

What are the treatment options for this patient? 

•  Topical clotrimazole, miconazole, tioconazole, butoconazole, econazole, terconazole, fenticonazole, nystatin. 
• Oral ketoconazole, itraconazole and fluconazole.
  
  

•  Oropharyngeal candidiasis (thrush), esophagitis, skin infections in moist areas, chronic mucocutaneous candidiasis associated with T cell defects, UTI, retinitis and endophthalmitis, catheter infections, endocarditis, rarely pneumonia and surgical wound infections.
  
  

• C krusei, C parapsilosis, C tropicalis, C guillermondii, C glabrata also known as Torulopsis glabrata.