CANDIDAL BALANITIS, YEAST INFECTION IN MEN – Symptoms, Causes, and Treatment

Yeast infections are often thought of as a female health problem, but men aren’t safe from these infections, either.

Yeast infections, or candidiasis, can affect other areas of the body:

• A yeast infection of the mouth is called thrush, or oral candidiasis.
• Infection of the skin (such as the armpits and groin) is called cutaneous candidiasis.
• Same infection of the penis –  which is inflammation of the head of the penis – is also called candidal (or candida) balanitis, or balanitis thrush.
• Common fungal infections of the foot are foot fungus, toenail fungus, toe infection.

In this article we focus on a yeast infection in men – a penile yeast infection, which may be a result of unprotected sex with a partner who has a vaginal yeast infection or also inadequate hygiene. Symptoms include redness on the skin and itchiness or burning.

With proper treatment, yeast infections mostly go within a few days. But not all the time and if so, the complications can be serious, even life-threatening.

What are the signs and symptoms of a yeast infection in men?

Men usually don’t experience yeast infection symptoms like women. However, once symptoms emerge, they may cause ultimate pain and discomfort. Symptoms may mimic other diseases, including some sexually-transmitted infections (STDs), so don’t ignore those symptoms once they appear.

To discover the reasons of the symptoms, men should always visit an urologist or primary care doctor who can diagnose the condition.

Symptoms of yeast infections in men include:

• Discomfort and burning (dysuria) during urination
• Itching or a burning sensation on the penis
• Moist skin on the penis, possibly with areas of a thick, white substance collecting in skin folds
• Sores on the foreskin of the penis
• Irritation, itchiness and pain at the tip of the penis
• White, lumpy, foul-smelling discharge
• Discomfort during sexual intercourse
• Redness and inflammation at the top of the penis
• Small rash like bumps that may contain pus
• Areas of white, shiny skin at the top of the penis

What causes a penile yeast infection?

The fungus that causes yeast infections (candida) is normally present on the body and skin. It is a is a everyday resident of even in the healthiest bodies. Therefore yeast infections in men are very common.

Candida loves moist, warm, and dark places, especially the genital area and gastrointestinal tract. The most common species is Candida albicans.

Candida normally lives innocently in these loved warm and moist places in your body and your microbiota keeps it from taking over (Lactobacillus bacteria keeps its growth in check). However, if there’s an imbalance in your microbiota (for example you suffer from dysbiosis) or you have had sex with infected partner, candida can start to overgrow. And a moist conditions are perfect for candida to spread.

Candida albicans overgrowth can affect both – men, as well as women.

Yeast infection is not sexually-transmitted disease (STD). However, it is possible that infected woman spreads it to her male sex partner. Therefore, one of the most usual causes of a penile yeast infection is unprotected sex with a woman with candida overgrowth.

However, men can also develop the yeast infection without being sexually active.

Common causes and potential risk factors for male yeast infections include:

• Antibiotic use, which lower probiotic counts, allowing for the growth of candida
• Weakened immune systems due to illness and chronic health conditions, which allows candida to spread. If you have an impaired immune system because of cancer treatment, HIV, or another reason, you may also be at a higher risk of a yeast infection.
• Frequent sexual intercourse
• Poor hygiene
• Being uncircumcised
• Having diabetes, as men with diabetes have higher amount of sugar in their urine, which may promote the growth of yeasts
• Using soaps and skin products that irritate skin
• Wearing tight-fitting undergarments or wet clothing
• Condoms that contain lubricants
• Using spermicides
• Any exposure to a hot, humid environments
• Being overweight

What is the treatment for yeast infection in men?

In rare cases the mild yeast infections do not need treatment and the medicaments are not necessary unless the man develops symptoms. Even when left untreated, it might go away by itself. However, the yeast infection can sometimes spread to the scrotum, inner thighs and buttocks. Even more, serious penile yeast infection, if not treated, may lead to a wide scale of painful, uncomfortable, and potentially embarrassing symptoms. Also, severe infection can lead to dreadful complications if it spreads into bloodstream.

Fortunately, treatment for men with antifungal medications is simple. These medications come in topical (applied as cream) and oral form (in pill or tablet form).

Usually those medications are on sale as OTC medications (it means you don`t need prescription), and when used twice a day for about one to three weeks is mostly sufficient to cure the yeast infection.

However, men who suffer from yeast infection for the first time, and have not received a treatment before – should not self medicate themselves with OTC anti-fungal medications and should see a doctor.

From time to time yeast infections come back after they seem to be cured. If this happens, your doctor will probably suggest weekly treatments for several months. More severe, or longer-term yeast may need a prescription medicine.

If your yeast infection doesn’t respond to treatment and you are not uncircumcised, your doctor may suggest you to have a circumcision. This surgical procedure is commonly done on infants, however, it can be done safely on a man at any age.

Many of the antifungal creams or oral medications recommended for a yeast infection include:

• Miconazole (Lotrimin AF, Cruex, Desenex, Ting Antifungal)
• Imidazole (Canesten, Selezen)
• Clotrimazole (Lotrimin AF, Anti-Fungal, Cruex, Desenex, Lotrimin AF Ringworm)
• Oral Fluconazole (Diflucan) and a Hydrocortisone Cream may be advised in serious infections, for example for those who have developed a potentially serious condition called balanitis.

Usually people tolerate most antifungal creams well. You’re not likely to have any serious side effects. However, ask your doctor and pharmacist what to look out for in case you have a bad reaction.

Other treatment methods recommended for a yeast infection include:

• Along with using the medicated cream, you should also practice good hygiene which can help prevent yeast infections and even treat them. It is a good idea to wash the penis regularly with plain warm water, avoiding shower gels and soaps, and drying well after.
• Men should never use perfumed shower gels or soaps on their genitals.
• Wearing loose-fitting cotton underwear or boxers and keeping genitals dry and cool at all times can also prevent yeast growth.
• Although various herbal remedies have been touted for women with yeast infections, there’s no data on their efficacy (or lack thereof) in men. But, there is no harm in trying.
• If you have diabetes, work with your healthcare providers to make sure your blood sugar levels are well controlled.
• If you have a suppressed immune system, your doctor can recommend ways to help keep your immune system as healthy as possible. But there are also something you can do for the health of your immune system right now. This includes healthy food, enough physical activity, no stress and taking probiotics and vitamins like Vitamin D.

When men have got the infection because of unprotected sexual intercourse, both partners should receive treatment so they would not re-infect each other. There’s no reason to limit or avoid sex during treatment, however you should use a condom.

What are the complications of a penile yeast infection?

Penile yeast infection may lead to balanitis, which is an inflammation of the head or the foreskin of the penis. According to one report in the journal Clinical Microbiology Reviews, candida yeasts are blameworthy for up to 35 % of all the cases of balanitis.

Complications include:

• Untreated balanitis may lead to scarring of the foreskin.
• It can also cause adhesions on the penis. The condition can be painful and make urinating more difficult.
• If untreated, balanitis can cause swollen and painful glands, as well as weakness and fatigue.
• A yeast infection may enter the bloodstream (known as candidemia or invasive candidiasis). This is most common in men with weakened immune systems or who wait to receive treatment until the infection has spread beyond the penis.
• If you’ve been in a hospital and used a catheter to urinate, you may be more likely to face invasive candidiasis. This advanced form of a yeast infection is very serious. The treatment may include oral antifungal medications for several weeks. In some cases, the drugs are administered intravenously.
• Immunocompromised patients or patients who have undergone an invasive procedure (e.g., placement of a central venous line) with contaminated equipment may develop severe, even life-threatening yeast infections.

You may be more likely to develop balanitis from a yeast infection if you:

• Are uncircumcised
• Use antibiotics for prolonged periods
• Have diabetes
• Have an impaired immune system, such as with HIV
• Are overweight
• Practice poor hygiene

How do you prevent a penile yeast infection?

You can help prevent a penile yeast infection by avoiding unprotected sexual contact with a partner who has a yeast infection. Also keep away from unprotected sex with anyone while you have an yeast infection. Because you could give the infection back to your partner, and the two of you could swap it back and forth.

To avoid getting a yeast infection or passing one along, do the following:

• Wear a condom to help reduce your chances of developing a yeast infection.
• Practice sexual monogamy to reduce your risk for a yeast infection.
• Practice good hygiene, and keep your penis and genitals clean and dry.
• If you are uncircumcised, clean under the foreskin with soap and water, and return your foreskin to its usual position after you have sexual intercourse.
• Practice healthy lifestyle and keep your immune system strong. That includes nutrition diet full of probiotics and vitamins like Vitamin D.

NB! The information provided here is for informational purposes only, so do not consider it as health care or medical diagnosis and treatment. Do not consider this information as a guarantee of the results you want to achieve. In addition, this information does not replace the advice of your physician or other healthcare professional.

Even more, you should not use it to diagnose or treat a health problem. Before changing or discontinuing your existing medication, treatment, or care, or taking any dietary supplements, be sure to consult with your healthcare professional or doctor before starting any diet or program, or if you suspect you may have a medical condition.

Compiled by Maria-Helena Loik

Sources: Onemedical.com, Verywellhealth.com, Mayoclinic.org, Healthline.com, Everydayhealth.com, Tipsbulletin.com

Photos: Pexels.com, Pixabay.com

Fifty-five-year-old man with chronic yeast infections

• Journal List
• Allergy Asthma Proc
• PMC4147028

As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with,
the contents by NLM or the National Institutes of Health.

Learn more about our disclaimer.

Allergy and Asthma Proceedings

Allergy Asthma Proc. 2014 Sep-Oct; 35(5): 415–422.

doi: 10.2500/aap.2014.35.3776

, M.D.,¹, M.D., M. Eng.,², D.O.,², B.S.,³, B.A.,³, M.D.,³ and , M.D.²

Author information Copyright and License information Disclaimer

As immunologists, we are frequently asked to evaluate patients with recurrent infections. These infections can provide us with clues regarding what pathways might be aberrant in a given patient, e.g., specific pyogenic bacteria with Toll-like receptor problems, atypical mycobacteria with interferon gamma receptor autoantibodies, and Candida/staphylococcal infections with cellular immune abnormalities. We present a 55-year-old man who presented to our immunology clinic with onychodystrophy of the toenails and fingernails and recurrent oral–esophageal candidiasis. The differential diagnosis for recurrent yeast infections is complex and includes usual suspects as well as some that are not as straightforward.

Keywords: Antibody deficiency, autoantibodies, chronic mucocutaneous candidiasis, Good’s syndrome, IL-12, interferon alpha, thymoma

Chief Complaint

Onychomycosis and recurrent oral–esophageal candidiasis.

History of Present Illness

A 55-year-old man was referred to the University of Virginia Immunology Clinic for onychodystrophy of his fingernails and toenails and recurrent oral–esophageal candidiasis. He had the problem with his toenails since childhood, but this had subsequently spread to involve his fingernails ∼4–5 years ago. Six months previously, he was diagnosed with oral candidiasis and was successfully treated with nystatin. He had no history of antibiotic or corticosteroid usage. One week later, he again developed thrush, and this pattern continued over the next months. Concomitantly, he was evaluated by the Dermatology Department for the onychodystrophy. Fingernail cultures were positive for Candida and his toenails grew dematiaceous mold. He was treated with fluconazole or itraconazole at various times over the past year and noted improvement with these treatments. Again, once the medications were removed, his symptoms returned. His last course of antifungal medication was completed 2 weeks before presenting to our clinic.

During our evaluation, he reported early dysphagia, especially while eating bread. He also described symptoms of gastroesophageal reflux and cough that were persistent and exacerbated after both eating and exercising. The cough would resolve with his ongoing antiyeast treatments. He denied constitutional symptoms as well as sinopulmonary, gastrointestinal, blood, bone, central nervous system, or kidney infections. He denied recurrent herpes, varicella, or human papilloma virus infections. Most importantly, he denied infections with Staphylococcus aureus including furunculosis. He had no history of autoimmune disease such as thyroiditis, autoimmune hemolytic anemia, or idiopathic thrombocytopenic purpura, although he did report transverse myelitis that developed temporally to receiving the tetanus and influenza vaccinations, ∼17 years before presenting to our clinic. He had no human immunodeficiency virus (HIV) risk factors.

Physical Examination

On physical examination his oropharynx was without evidence of oral candidiasis. He had no lymphadenopathy and his respiratory exam was normal. Skin examination did not show atopic dermatitis or furunculosis; however, he had significant onychodystrophy of his fingernails and toenails.

Laboratory and Other Diagnostic Findings

Our initial immunologic evaluation showed absent delayed-type hypersensitivity testing to Candida and Trichophyton, at 48 hours. He was diagnosed with chronic mucocutaneous candidiasis (CMC). His complete blood count revealed normal numbers of neutrophils, lymphocytes, and monocytes, but, interestingly, he had no eosinophils or basophils (). Flow cytometry () showed a low CD4:CD8 ratio with low–normal absolute CD4 T-cell numbers (585/μL) but was very surprising for the complete absence of CD19 B cells. The absence of B cells was subsequently confirmed with enumeration of CD20 cells, which were also absent. Because of the absence of B cells, quantitative immunoglobulins were measured and, along with specific antibody testing, these were surprisingly unremarkable ().

Table 1

Patient characteristics from our initial immune workup

Open in a separate window

Abs = absolute; H = high; L = low; HIV = human immunodeficiency virus; CBC = complete blood count; WBC = white blood cell count.

Clinical Course

A chest computed tomography scan showed the presence of a large anterior mediastinal mass. He was referred to thoracic surgery for video-assisted thoracoscopy with thymectomy. Pathology showed a noninvasive type B1 thymoma with a lymphocytic predominance but no spindle cells. A repeat computed tomography chest scan at 6 months follow-up did not reveal recurrence of his anterior mass. Interestingly, IgG levels have remained normal postthymectomy and IgG level at 6-month follow-up was 921 mg/dL.

What Is the Differential Diagnosis of CMC?

CMC is the result of the failure of T lymphocytes to mount a cellular immune response to Candida, leading to chronic Candida infections that are typically limited to mucosal surfaces, skin, and nails. CMC can present as a manifestation of a wide number of underlying conditions. Most commonly, CMC is a component of the myriad of infections associated with the comprehensive loss of T-cell function that occurs, e.g., in severe combined immune deficiency, DiGeorge syndrome, HIV, etc. Any patient with CMC should be HIV tested. In addition to negative viral load, our patient had normal numbers of CD4 T cells (), which, along with his age, eliminated severe combined immune deficiency or other acquired or idiopathic CD4 lymphopenias as a mechanism for his disease.

The immune response to Candida requires complex interactions between immune cells and the yeast for adequate recognition, engagement of innate and adaptive immune responses, phagocytosis, and killing. Innate immunity includes a combination of monocytes, macrophages, neutrophils, dendritic cells, and others that together maintain homeostasis with this usual commensal organism, using Toll-like receptors (TLR2 and 4), complement receptors (CR3), and numerous pattern recognition receptors, such as the C-type lectin receptors (CLR; macrophage mannose receptor, Dectin-1, DC-sign, etc.) that are necessary for recognition of mannans and mannoproteins within the cell walls of Candida albicans.¹ For the development of adaptive, largely Th27-mediated immunity, binding of Dectin-1 on the surface of dendritic cells signals the CARD9 complex, ultimately activating the production of cytokines including transforming growth factor (TGF) β, IL-6, and IL-23. ² These cytokines provide “signal 3” for the adjacent T cells, which are simultaneously having Candida antigen presented by the dendritic cells. In the context of cellular differentiation, signal 1 refers to major histocompatibility complex/T-helper cell interactions, and signal 2 refers to costimulatory molecules CD80/86 integrating with their respective ligands. Signal 3 represents the cytokine milieu that supports T-cell activation and promotes T-helper immune deviation. In the generation of Th27 cells, the cytokine milieu required includes TGF-β, IL-6, and IL-23. These cytokines signal through tyrosine kinase 2 (Tyk2) to activate the nuclear transcription factor STAT3. These signaling molecules and, especially, STAT3, lead to the production of IL-17 and the differentiation of Th27 cells.^3,4 Mutations in genes encoding these proteins and others can lead to Th27 deficiencies and the diagnosis of CMC (; ).

Table 2

Differential diagnosis for CMC

Open in a separate window

Open in a separate window

AR = autosomal recessive; CMC = chronic mucocutaneous candidiasis; IFN = interferon.

Open in a separate window

Genetic- and autoantibody-associated mechanisms of chronic mucocutaneous candidiasis (CMC). See text for details. Red boxes designate potential genetic mutations associated with CMC, and blue boxes represent putative autoantibodies.

STAT3-deficient (hyper-IgE syndrome) patients are defined by their markedly elevated IgE levels and, in further contrast to this patient, are generally hypereosinophilic and show susceptibility to skin and respiratory Staphylococcus infections (along with the candidiasis).⁵ Mutations in dedicator of cytokinesis 8 (Dock8) and Tyk2 are also characterized by elevated serum IgE levels, eosinophilia, sinopulmonary staph infections, and lymphopenia along with the CMC. These are autosomal recessive (AR) conditions that are largely distinguished from autosomal dominant hyper-IgE syndrome by the presence of frequent cutaneous viral infections and defects in humoral immunity (e.g., low IgM).^6–10

IL-17F deficiency is an autosomal dominant condition in which the host displays impaired (but not abolished) activity against Candida, possibly reflecting the continuing presence of IL-17A. In contrast, IL-17RA deficiency is an AR condition that completely abolishes cellular responses to both IL-17A and IL-17F¹¹ and thereby produces a much more severe defect in anti-Candida immunity. Complete STAT1 deficiency leads to diminished STAT1-dependent cellular responses to both interferon (IFN) α/β as well as IFN-γ. Patients with this disease suffer from both severe viral infections (herpes viruses), as well as intracellular pathogens (Salmonella, BCG, and nontuberculous mycobacteria).¹² Interestingly, gain of function autosomal dominant STAT1 mutations can develop infections similar to those with loss of function mutations but can also develop infections with dimorphic molds (Samplaio et al.¹³) as well as CMC and autoimmunity (Uzel et al.¹⁴). Although these patients have increased expression of cytokines that promote Th27 immune deviation (IL-6 and IL-21), ultimately, the stronger cellular responses to the STAT-1 activating cytokines IFN-α/β, IFN-γ, and IL-27 prevail, and their Th2 immune deviating influences supersede and hinder the development of Th27 cells. ¹⁵ STK4 deficiency was described in a cohort with T and B lymphopenia and histories of multiple bacterial and viral infections (especially cutaneous human papilloma virus), along with CMC¹⁶ (; ).

CARD9 is an important part of the pathway engaged by the pattern recognition receptor Dectin-1, which is responsible for initiating many innate immune responses to fungal elements, including, ultimately, the development of Th27 cells as discussed previously.¹⁷ Consistent with its essential role as a “danger signal” capable of recognizing Candida-derived fungal elements AR mutations in Dectin-1 and CARD9 have also been associated with the CMC phenotype. However, CARD9 defects are associated less with CMC but instead with severe invasive Candida infections, including meningitis¹⁸ (; ).

Finally, autoimmune polyendocrinopathy ectodermal dystrophy results from AR mutations of the autoimmune regulator gene, which in contrast to our patient, is typically characterized by autoimmune hypoparathyroidism and adrenal insufficiency, along with CMC. ¹⁹ CMC in this population has been linked to presence of autoantibodies against IL-17A, IL-17F, and IL-22,^20,21 although diminished intrinsic Th27 responses have also been established.²⁰

How Does the Finding of Absent B Cells Affect This Differential?

Absence of B lymphocytes can be seen in numerous conditions and in association with use of rituximab (anti-CD20 antibodies; ). After we discovered our patient had no B cells, we broadened our differential diagnosis to include adult onset X-linked agammaglobulinemia caused by forme fruste mutations in the BTK gene. However, these B-cell deficiencies are not typically associated with CMC, and he lacked any of the typical presenting features suggestive of a humoral immune deficiency. As such, the most likely etiology of his acquired B-cell deficiency is Good’s syndrome. Good’s syndrome is a rare, adult-onset primary immunodeficiency, characterized by low or absent B cells, hypogammaglobulinemia, and multiple autoimmune diseases in the setting of an underlying thymoma. As with our patient, Good’s syndrome patients usually exhibit relative CD4 T-cell lymphopenia (low–normal in our patient), absent eosinophils and basophils, and present in the 4–5th decade of life.^22,23 Additionally, our patient presented with symptoms concerning for a mediastinal process (difficulty swallowing). However, Good’s syndrome requires deficient IgG antibodies, and, at the time of evaluation, our patient’s immunoglobulins were normal, which is inconsistent with this diagnosis (see discussion later in text).

Table 3

Differential diagnosis for absent B cells

Open in a separate window

AR = autosomal recessive.

What Additional Investigations Would Be Helpful in This Patient to Determine How His Thymoma Produced CMC?

After informed consent, blood samples were taken from the patient. Flow cytometry was performed in the research laboratory at the National Institutes of Health to measure CD4⁺ T cells expressing intracellular IL-17A, identification markers for Th27 cells. Our patient showed absent Th27 cells compared with the control (3.12%;
A). Because patients with thymoma develop numerous autoantibodies that produce a myriad of autoimmune diseases ()^20,24–26 presumably reflecting the role of the thymus in negative selection of autoreactive cells, we hypothesized that our patient would have autoantibodies to IL-17. We worked with our partners at the National Institutes of Health to evaluate for anticytokine autoantibodies. These studies showed autoantibodies to IFN-α, IFN-ω, IFN-λ3, and IL-12p70 but not to IL-17 (including A and F) or IL-22 (
B). Further testing revealed no evidence of autoantibodies to granulocyte–colony-stimulating factor, granulocyte macrophage–colony-stimulating factor, IFN-β, IFN-γ, TNF-β, IFN-γ-inducible protein (CXCL10; IP-10), IL-4, IL-6, or IL-15.

Open in a separate window

Evidence of Th27 deficiency by flow cytometry and autoantibodies. (A) IL-17a production (%) in CD4⁺ memory T cells (red circles) for normal (top panels) and patient peripheral blood mononuclear cells pre- and postthymectomy (middle and lower panels, respectively). Unstimulated (left panels) or stimulated with phorbol 12-myristate 13-acetate/ionomycin (right panels) conditions. (Right side of each panel shows interferon [IFN] γ–producing CD4⁺ memory T cells.) Unstimulated condition not available for prethymectomy sample because of lymphopenia. B) Anticytokine autoantibodies before and after thymectomy. Plasma was mixed with the cognate beads, washed, and tested against human IgG.

Table 4

Anti-cytokine antibodies and their associated diseases

Open in a separate window

IFN = interferon; CMC = chronic mucocutaneous candidiases; G-CSF = granulocyte–colony-stimulating factor; GM-CSF = granulocyte cacrophage–colony-stimulating factor; SLE = systemic lupus erythematosus.

Autoantibodies to IL-17 are thought to be one cause of CMC associated with thymoma, reflecting the subsequent loss of the ability of Th27 cells to carry out their anticandidal (and antibacterial) immune functions.^20,25 However, the absence of Th27 cells in our patient could be a reflection of defective T-cell development secondary to thymic dysfunction or could also be ascribed to autoantibodies to cytokines essential for Th27 immune development. Although IL-6 and TGF-β are the most important cytokines necessary for the generation of Th27 cells, other cytokines including IL-23 contribute. IL-23 is a heterodimer consisting of a unique IL-23α chain and the p40 chain of IL-12.²⁷ Thus, autoantibodies to anti–IL-12 are capable of also targeting IL-23. We hypothesize that this could explain our patient’s depressed Th27 immunity (). Although we recognize that anti–IL-12p40 autoantibodies are prevalent in thymoma, without necessarily resulting in CMC,²⁸ it is also likely that anticytokine autoantibodies can manifest differently,²⁹ possibly depending on host and environmental factors, as well as differences intrinsic to the autoantibodies themselves.

Open in a separate window

The role of autoantibodies to IL-12 in the development of chronic mucocutaneous candidiasis (CMC). The shared subunit p40 allows for antibody blockade of both Th2 responses via IL-12 and Th27 responses via IL-23. See text for details.

We speculated that as with other autoimmune syndromes associated with thymoma (e.g., myasthenia gravis), thymectomy might be associated with loss of his autoantibodies and restoration of his Th27 compartment. Because it is unknown if or even whether this could occur, we decided to start the patient on continuous fluconazole as prophylaxis. However, 1 year after thymectomy, we repeated anticytokine autoantibody testing, and it appears that the autoantibodies persisted against IFN-α IFN-ω, IFN-λ3, and IL-12p70 (
B). At this time, he remains on antifungal prophylaxis to manage his infections.

Surprisingly, despite his absence of B cells, our patient had normal immunoglobulins, reflecting the ongoing presence of long-lived plasma cells. The life expectancy of human plasma cells is presently not known. However, we can expect that at some time in the future he will become the “typical” Good’s syndrome patient and develop humoral immune failure. Furthermore, on biopsy, our patient did not have the typical histological finding in the thymus of spindle cells that are associated with Good’s syndrome. However, spindle cells are not required for the diagnosis of Good’s syndrome, and other cell types within the thymoma have been described, including epithelial cell tumors and/or mixed epithelial/lymphoid tumors.²²

The absence of B cells in this disease is thought to also reflect an autoimmune process but, once the B-cell compartment is destroyed, this can never be restored even if these autoantibodies also resolve, presumably reflecting the absence of B lymphocyte stem cells. Although the timing of his humoral immune failure remains unclear, our patient will be monitored closely for infections and will have yearly quantitative antibody titers because we expect him to ultimately need to start replacement immunoglobulin therapy.

Final Diagnosis

This patient has a thymoma associated with autoantibodies to IFN-α and IL-12p70 and CMC. It is possible that his illness may progress in the future to be Good’s syndrome.

JL Kennedy received Grants- KL2TR000063; UL1TR000039, ARTrust Minigrant, COBRE pilot project grant 1P20GM103625–02. The remaining authors have no conflicts of interest to declare pertaining to this article

1.
Netea MG, Brown GD, Kullberg BJ, Gow NA.
An integrated model of the recognition of Candida albicans by the innate immune system. Nat Rev Microbiol
6:67–78, 2008. [PubMed] [Google Scholar]

2.
Brown GD.
Dectin-1: A signalling non-TLR pattern-recognition receptor. Nat Rev Immunol
6:33–43, 2006. [PubMed] [Google Scholar]

3.
Iwakura Y, Ishigame H.
The IL-23/IL-17 axis in inflammation. J Clin Investig
116:1218–1222, 2006. [PMC free article] [PubMed] [Google Scholar]

4.
Kimura A, Kishimoto T.
IL-6: Regulator of Treg/Th27 balance. Eur J Immunol
40:1830–1835, 2010. [PubMed] [Google Scholar]

5.
Chandesris MO, Melki I, Natividad A, et al.
Autosomal dominant STAT3 deficiency and hyper-IgE syndrome: molecular, cellular, and clinical features from a French national survey. Medicine
91:e1–19, 2012. [PMC free article] [PubMed] [Google Scholar]

6.
Renner ED, Puck JM, Holland SM, et al.
Autosomal recessive hyperimmunoglobulin E syndrome: A distinct disease entity. J Pediatr
144:93–99, 2004. [PubMed] [Google Scholar]

7.
Zhang Q, Davis JC, Lamborn IT, et al.
Combined immunodeficiency associated with DOCK8 mutations. New Engl J Med
361:2046–2055, 2009. [PMC free article] [PubMed] [Google Scholar]

8.
Watford WT, O’Shea JJ.
Human tyk2 kinase deficiency: Another primary immunodeficiency syndrome. Immunity
25:695–697, 2006. [PubMed] [Google Scholar]

9.
Minegishi Y, Karasuyama H.
Hyperimmunoglobulin E syndrome and tyrosine kinase 2 deficiency. Curr Opin Allergy Clin Immunol
7:506–509, 2007. [PubMed] [Google Scholar]

10.
Minegishi Y, Saito M, Morio T, et al.
Human tyrosine kinase 2 deficiency reveals its requisite roles in multiple cytokine signals involved in innate and acquired immunity. Immunity
25:745–755, 2006. [PubMed] [Google Scholar]

11.
Puel A, Cypowyj S, Bustamante J, et al.
Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity. Science
332:65–68, 2011. [PMC free article] [PubMed] [Google Scholar]

12.
Chapgier A, Kong XF, Boisson-Dupuis S, et al.
A partial form of recessive STAT1 deficiency in humans. J Clin Investig
119:1502–1514, 2009. [PMC free article] [PubMed] [Google Scholar]

13.
Sampaio EP, Hsu AP, Pechacek J, et al.
Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis. J Allergy Clin Immunol
131:1624–1634, 2013. [PMC free article] [PubMed] [Google Scholar]

14.
Uzel G, Sampaio EP, Lawrence MG, et al.
Dominant gain-of-function STAT1 mutations in FOXP3 wild-type immune dysregulation-polyendocrinopathy-enteropathy-X-linked-like syndrome. J Allergy Clin Immunol
131:1611–1623, 2013. [PMC free article] [PubMed] [Google Scholar]

15.
Liu L, Okada S, Kong XF, et al.
Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis. J Exp Med
208:1635–1648, 2011. [PMC free article] [PubMed] [Google Scholar]

16.
Abdollahpour H, Appaswamy G, Kotlarz D, et al.
The phenotype of human STK4 deficiency. Blood
119:3450–7347, 2012. [PMC free article] [PubMed] [Google Scholar]

17.
Gross O, Gewies A, Finger K, et al.
Card9 controls a non-TLR signalling pathway for innate anti-fungal immunity. Nature
442:651–656, 2006. [PubMed] [Google Scholar]

18.
Glocker EO, Hennigs A, Nabavi M, et al.
A homozygous CARD9 mutation in a family with susceptibility to fungal infections. New Engl J Med
361:1727–1735, 2009. [PMC free article] [PubMed] [Google Scholar]

19.
Proust-Lemoine E, Saugier-Veber P, Wémeau JL.
Polyglandular autoimmune syndrome type I. Presse Med
41:e651–e662, 2012. [PubMed] [Google Scholar]

20.
Kisand K, Bøe Wolff AS, Podkrajsek KT, et al.
Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th27-associated cytokines. J Exp Med
207:299–308, 2010. [PMC free article] [PubMed] [Google Scholar]

21.
Puel A, Döffinger R, Natividad A, et al.
Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I. J Exp Med
207:291–297, 2010. [PMC free article] [PubMed] [Google Scholar]

22.
Kelleher P, Misbah SA.
What is Good’s syndrome? Immunological abnormalities in patients with thymoma. J Clin Pathol
56:12–16, 2003. [PMC free article] [PubMed] [Google Scholar]

23.
Mitchell EB, Platts-Mills TA, Pereira RS, et al.
Acquired basophil and eosinophil deficiency in a patient with hypogammaglobulinaemia associated with thymoma. Clin Lab Haematol
5:253–257, 1983. [PubMed] [Google Scholar]

24.
Browne SK, Holland SM.
Anticytokine autoantibodies in infectious diseases: Pathogenesis and mechanisms. Lancet Infect Dis
10:875–885, 2010. [PubMed] [Google Scholar]

25.
Burbelo PD, Browne SK, Sampaio EP, et al.
Anti-cytokine autoantibodies are associated with opportunistic infection in patients with thymic neoplasia. Blood
116:4848–4858, 2010. [PMC free article] [PubMed] [Google Scholar]

26.
Meager A, Wadhwa M, Dilger P, et al.
Anti-cytokine autoantibodies in autoimmunity: Preponderance of neutralizing autoantibodies against interferon-alpha, interferon-omega and interleukin-12 in patients with thymoma and/or myasthenia gravis. Clin Exp Immunol
132:128–136, 2003. [PMC free article] [PubMed] [Google Scholar]

27.
Oppmann B, Lesley R, Blom B, et al.
Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity
13:715–725, 2000. [PubMed] [Google Scholar]

28.
Meager A, Vincent A, Newsom-Davis J, Willcox N.
Spontaneous neutralising antibodies to interferon-alpha and interleukin-12 in thymoma-associated autoimmune disease. Lancet
350:1596–1597, 1997. [PubMed] [Google Scholar]

29.
Sim BT, Browne SK, Vigliani M, et al.
Recurrent Burkholderia gladioli suppurative lymphadenitis associated with neutralizing anti-IL-12p70 autoantibodies. J Clin Immunol
33:1057–1061, 2013. [PubMed] [Google Scholar]

Articles from Allergy and Asthma Proceedings are provided here courtesy of OceanSide Publications

Microflora of the urogenital tract in men examined for chronic prostatitis

Treatment of chronic inflammatory pathology of the urogenital tract in men has always been a difficult task in urology. Treatment for these diseases, especially those complicated by impaired fertility, sexual dysfunction, pelvic pain syndrome, can be successful if done individually and based on knowledge of the etiology of the inflammatory process, immunoreactivity to this inflammatory process and morphological and functional changes in the pelvic organs.

In wide medical practice, at present, when diagnosing the etiological factor of the inflammatory pathology of the urogenital tract, the emphasis is on identifying sexually transmitted infections. The purpose of this study is to demonstrate the significance of other equally important etiological factors, as well as the place of STIs in the pathogenesis of this group of inflammatory diseases. Infectious inflammatory process in the urogenital tract occurs by two mechanisms.

In the first case, a virulent STI causes clinically and laboratory identifiable urethritis, which subsequently leads to an ascending inflammatory process. The pathogenetic role of a sexually transmitted infection in this case is obvious: when examining discharge from the urethra, prostate secretion, seminal fluid, a significant increase in the number of leukocytes and STIs is detected; the primary inflammatory process begins with the clinic of urethritis. Patients with an inflammatory process of this nature are most often treated in dermatovenerological dispensaries, when, in addition to an acute venereal disease, there is a prostatitis clinic.

The second mechanism is more complex. The occurrence of an infectious inflammatory process in the urogenital tract in this case is preceded by certain predisposing factors.

We single out several main groups:

1. The first group of factors includes vascular, trophic and morpho-functional changes in the pelvic organs, which occur as a result of congestion in the pelvic organs, habitual intoxications and other causes. These changes are well known and have been widely discussed in special Russian literature.
2. Infravesical obstruction is also a predisposing cause of infectious inflammation. In this case, there is a retrograde flow of urine into the acini of the prostate gland at the time of urination due to an increase in intraurethral pressure. This can lead to infection of the prostate gland with microflora from the overlying urinary tract.
3. The most important predisposing cause of the inflammatory process of the urogenital tract is secondary immunodeficiency, which develops against the background of a sluggish intracellular bacterial infection (chlamydia, mycoplasma) and a persistent viral infection (urogenital herpes, cytomegalovirus). Infection of the urogenital tract with this microflora leads to a characteristic violation of phagocytic activity (HCT test), a decrease in class A immunoglobulins with an increase in class G immunoglobulins; violation of T helper and T suppressor interactions. Secondary immunodeficiency, as well as certain morphological and functional changes in the pelvic organs, open the way to infection of the urogenital tract with banal pathogenic and opportunistic bacterial microflora.

With the development of an infectious process in the urogenital tract according to this mechanism, there is no clinic of urethritis, there will be no significant increase in the number of leukocytes in studies of discharge from the urethra, STIs will be detected in scrapings from the urethra much less frequently, however, patients will have a clinically and laboratory identifiable inflammatory process in the prostate-vesicular complex or in the organs of the scrotum.

In the presence of the above predisposing factors, infection of the urogenital tract with banal bacterial microflora is fundamentally possible in two ways: transurethral and hematogenous.

Hematogenous infection most often occurs from foci of chronic infection with concomitant ENT pathology, diseases that have the widest distribution in the population; with diseases of the rectum with chronic constipation, hemorrhoids (especially with frequent exacerbations). Infection along this route most often occurs when there are already pronounced structural changes in the prostate gland ( congestion, calcifications, BPH).

The transurethral route of infection with secondary bacterial microflora is more significant. Four main sources of bacterial infection should be identified.

1. Widespread bacterial vaginosis in women. According to the Preobrazhensky Clinic, women examined for inflammatory diseases of the genital organs were found to have bacterial vaginosis in 20% of cases. The cause of bacterial vaginosis is a small opportunistic rod flora, which often leads to infection of the urogenital tract of men. The cause of bacterial vaginosis is sluggish bacterial and persistent viral infections, hormonal disorders and other causes that cause secondary immunodeficiency. In married couples in women suffering from bacterial vaginosis, husbands are much more likely to have chronic prostatitis than in women with inflammatory gynecological diseases, but not having bacterial vaginosis.

Table of microorganisms most commonly found in the genitals of women in inflammatory diseases caused by gardnarella vaginalis and non-spore-forming bacteria. (collection of works of UrNIIDVII, 1985)

2. The prevalence of oral-genital and anal intercourse is also a source of infection of the urogenital tract of men. In the first case, infection occurs mainly with streptococcal or staphylococcal microflora, in the second case – with Gr-rod flora (Proteus, Klebsiella, Escherichia coli, etc.).

Clinical case.

Patient N13603 Igor Nikolaevich, 30 years old applied on 16. 05. 98 years old with complaints of pelvic pain. Examined at UrNIIDVII for the presence of STIs – gonorrhea, trichomoniasis, candidiasis, gardnarellosis, chlamydia, ureaplasmosis, mycoplasmosis, HSV were not found, in the prostate secretion of leukocytes 20-40-80 in p / s, there are no data for extragenital inflammatory pathology. Performed bacteriological examination of prostate secretion. Staphylococcus with hemolysis and Gr+ bacillus with hemolysis TMP 10×9 were detectedin 1 ml of discharge. Upon additional questioning, it was found that oral-genital sex is regularly practiced in the family, and the spouse suffers from chronic tonsillitis and sinusitis with frequent exacerbations. The wife (N13784 Anna Sergeevna, 29 years old) was referred to an otolaryngologist. In a bacteriological study of washings from the tonsils, staphylococcus aureus with hemolysis, Gr+ bacillus with hemolysis, TMC 10×6 in 1 ml of discharge were detected, the presence of chronic tonsillitis and sinusitis in the subacute phase was confirmed.

3. Iatrogenic infection with hospital microflora during urethral medical or diagnostic procedures, which are currently widespread.
4. Infection from the upper urinary tract and bladder, especially in the presence of bladder outlet obstruction.

The mechanism of development of bacterial inflammation in the urogenital tract is shown below, when it is not caused by sexually transmitted infections.

The purpose of this work was to analyze the microflora in patients examined for chronic prostatitis. In addition to testing for STIs in 1996-98, more than 200 bacteriological cultures were performed in men in the Preobrazhensky Clinic for various indications.

Bacteriological examination of the prostate secretion is carried out on the basis of the bacteriological laboratory of UrNIIDViI. Before taking the material, the patient is asked to empty the bladder and perform the toilet of the glans penis and preputial sac. Next, the prostate gland is massaged, its secret is placed in a test tube with an accumulation medium – sugar broth. Test tubes in a thermostat are delivered to the bacteriological laboratory within 40-60 minutes, where the material is immediately dispersed into 4 nutrient media: meat-peptone agar, blood agar, Endo medium and Sabur medium. After 24 hours, for further identification of the pathogen, subculturing is performed on the appropriate nutrient media (for example, to identify staphylococcus aureus in vitelline-salt agar to assess lyceto-vitellase activity, to blood plasma to assess plasma-coagulating activity). After 5 days, the results are “read”, pure cultures are subcultured on media with disks impregnated with antibacterial drugs, and after a day the antibiogram is “read”.

The study group included only those patients who, in the presence of clinical and laboratory data for the inflammatory process in the prostate-vesicular complex, did not have any data for inflammation in the urethra, they met the following conditions.

1. Minimum examination scope: smear analysis, examination of prostate secretion, examination for chlamydia, ureaplasmosis, mycoplasmosis, chronic gonorrhea, blood for HIV, RW, bacteriological examination of prostate secretion, ultrasound of the prostate with a transrectal probe.
2. The entire examination complex was completed within no more than 14 days.
3. Absence of a clinical picture of urethritis, and in the study of leukocyte discharge from the urethra, less than 10 per field of view.
4. Wessermann negative and no HIV.

Thus, in the study group there were 63 patients in the bacteriological study of the prostate secretion of which 113 microorganisms were isolated. The age of the patients ranged from 20 to 65 years. Let us note a certain regularity of the total degree of leukocytosis in the secretion of the prostate gland in patients of different age groups.

In the first age group, due to the fact that the inflammatory process began relatively recently, leukocytosis is still quite moderate. In the second group, where the history of the inflammatory process is already long, and the immune response to the inflammatory process is quite active, leukocytosis is the highest among the presented groups. In the third and fourth groups, despite the pronounced structural changes in the prostate gland, leukocytosis again decreases. This may be due to a significant decrease in the immune response during a long-term chronic inflammatory process.

The structure of the revealed microflora in the bacteriological study of the secretion of the prostate gland is presented in Table N1.

The data of the performed study must be evaluated with a high degree of criticality for the following reasons:

• This laboratory does not have an anaerobic balloon for performing inoculation under anaerobic conditions, therefore, the number of anaerobic microorganisms should be much larger.
• A significant growth of opportunistic microflora sometimes closes the true causative agent of inflammation. With repeated bacteriological examination after treatment, pathogenic microflora is sown much more often. However, this topic is outside the scope of this work.

Both pathogenic and opportunistic microorganisms have been identified. The ratio of pathogenic and conditionally pathogenic microorganisms is presented in the diagram.

Microorganisms were sown both as a monoinfection and in associations, which is presented in Table N2.

Thus, it can be seen that in 68.2% of cases in the bacteriological study of the secret of the prostate, associations of microorganisms are sown. It should be noted that in 46% of the examined (those 29of 63 patients) in the secretion of the prostate gland, microorganisms causing hemolysis of blood agar were detected, and the higher the degree of association, the more often a hemolytic microorganism is detected in its structure. More than half of patients are diagnosed with STIs, and their detection rate remains almost the same for any degree of association.

These data are presented in Table N2.

Table N3 shows the revealed hemolytic microflora:

The presented diagram shows that the detection of staphylococcal microflora prevails, which corresponds to the general layout of the detected microflora. The second place is occupied by Gram+ rod flora (unidentified Gr+ bacillus and corynobacteria), the third place is taken by streptococcus. Separately, we note that a certain part of the Gram-rod flora also exhibits hemolytic activity (12.5% ​​of the total number of detected Gram-bacteria).

We classified all other microorganisms as conditionally pathogenic microflora. We decided not to isolate microorganisms from this group, which can be considered rather as saprophytes. In our opinion, it is necessary to attribute this or that microorganism to the category of saprophytic microflora individually, taking into account all the data of clinical and laboratory diagnostics.

Conditionally pathogenic microflora is presented in Table N4.

According to the structure of pathogenic and opportunistic microflora, it is easy to see that the detected coccal microflora, especially streptococcal, is also characteristic of chronic diseases of the oral cavity. Gr+ and Gr-rod microflora are a frequent causative agent of bacterial vaginosis in women, in addition, Gr-rod is often a hospital microflora and an infection detected in chronic inflammatory diseases of the urinary system.

In 33 patients i.e. STIs were found in 52.4% of those examined in the absence of clinical and laboratory signs of an inflammatory process in the urethra.

Identified STIs are presented in Table N5.

Gonorrhea was identified in the study of scrapings from the urethra by the PCR method.

Yeast cells were detected during microscopic examination of discharge from the urethra or in bacteriological examination of prostate secretion with identification to the species. Chlamydia was identified in the study of scrapings from the urethra by PCR or PIF or in the presence of class M immunoglobulins to infection. Ureaplasmosis and mycoplasmosis were identified in the study of scrapings from the urethra by PCR. HSV and CMV were identified in the study of scrapings from the urethra by PCR or in the presence of class M immunoglobulins to infection.

A comparative analysis of the detection of STIs in patients in two groups was carried out:

Group 1 – there is a pathogen in bacteriological culture of prostate secretion, group 2 – only opportunistic microflora is detected in bacteriological culture.

The obtained data are presented in Table N6.

Thus, it can be seen that candidiasis, ureaplasmosis, mycoplasmosis, viruses are detected equally in both groups. But in the group with pathogenic microflora, gonorrhea and chlamydia are detected much more often. In practice, in patients with clinical and laboratory data of the inflammatory process in the prostate-vesicular complex and in the presence of chlamydia, hemolytic bacterial microflora is always sown!!!

Another reason why this work was done is demonstrated by the data in the following diagram.

Conclusions:

1. In all patients examined for chronic prostatitis in the absence of clinical and laboratory data of acute or chronic urethritis, bacteriological examination of prostate secretion revealed nonspecific bacterial microflora. In 46% of patients (in 29 out of 63 people), pathogenic (hemolytic) microflora was detected.
2. Conditionally pathogenic microflora was detected in 54% of patients, the pathogenicity of this microflora is assessed based on the specific clinical situation, taking into account all examination data.
3. In 68% of cases, microorganisms were sown in associations. Moreover, the higher the degree of association, the more often a microorganism with hemolytic activity was determined in it.
4. The structure of the bacterial microflora of the urogenital tract in men (both with and without hemolytic activity) suggests its possible source is bacterial vaginosis and diseases of the oral cavity in sexual partners, and also, possibly, the hematogenous route of infection.
5. Sexually transmitted infections were detected in 52.4% of patients in the absence of clinical and laboratory data of acute or chronic urethritis.
   Moreover, in cases where gonococci or chlamydia were detected in scrapings from the urethral mucosa by the PCR method, hemolytic microflora was determined during bacteriological examination of the prostate secretion.
6. Given the rather pronounced resistance of the identified microflora to antibacterial drugs, it is indicated to include bacteriological culture of prostate secretion in the program for examining patients with inflammatory diseases of the urogenital tract.

Zhuravlev V.N., Vlasenko L.Yu., Pankov V.I.

Candidiasis

Candidiasis of the mucous membranes of the urogenital tract is caused by yeast-like fungi of the genus Candida, the most common and pathogenic representative of which is C.albicans (up to 75–85% of cases). In the remaining 15-25% of cases, candidiasis is caused0430 C. kefyr . Fungi of the genus Candida colonize the mucous membranes of the gastrointestinal tract, oral cavity, urogenital tract and skin surface in a significant number of healthy people without causing the development of a pathological process. However, in persons with congenital or acquired immunity disorders, hormonal imbalance or long-term use of antibacterial drugs, yeast-like fungi may actively multiply, which disrupts the balance of microflora and leads to the development of an infectious-inflammatory process. Urogenital candidiasis in men occurs in the form of balanoposthitis and urethritis, causing inflammation of the foreskin, glans penis and anterior urethra. In women, the most common form of urogenital candidiasis is vulvovaginal candidiasis, accompanied by inflammation of the vaginal and vulvar mucosa and vaginal discharge. The inflammatory process can spread to the mucous membrane of the urethra and bladder. In about 5% of women, vulvovaginal candidiasis becomes recurrent (4 or more episodes per year).

Indications for examination. In men: dysuria, itching in the anterior urethra, foreskin; hyperemia and swelling of the glans penis, often with a white coating.

In women: symptoms of inflammation of the lower urogenital tract; pathological discharge from the vagina; pain during sexual intercourse.

Differential diagnosis. Urogenital trichomoniasis, bacterial vaginosis, aerobic vaginitis, chlamydial, gonococcal infection, infection due to M. genitalium .

Etiological diagnosis includes visual detection of blastospores and pseudomycelium of yeast-like fungi using microscopy, isolation of culture Candida with species identification, detection of DNA C.albicans and other species of the genus Candida .

Research material

• Vaginal swabs/scrapes for diagnosing vaginitis;
• Swabs/scrapings from the mucous membrane of the urethra and/or foreskin – for the diagnosis of urethritis and balanoposthitis.

Comparative characteristics of laboratory diagnostic methods. Visual detection of blastospores and pseudomycelium of yeast-like fungi of the genus Candida is carried out in native or fixed preparations, stained with methylene blue or Gram, using light microscopy. Microscopic examination is the most commonly used method for diagnosing candidiasis, as it allows you to detect the vegetative form of fungi – pseudomycelium (with the exception of C.glabrata ), as an additional diagnostic sign of the development of an infectious process. The disadvantage of the method is subjectivity and possible errors in the interpretation of the result, the impossibility of species identification, as well as low diagnostic sensitivity – 30–40%. To increase the sensitivity and specificity of the study, the preparation is treated with a 10–30% KOH solution before microscopy, in which case pseudomycelium and blastospores acquire greater contrast, the sensitivity of the method in manifest forms of candidiasis increases to 60–80%.

Sowing the sample on solid nutrient media is used to isolate the culture of fungi of the genus Candida . The study allows you to determine the type of fungus, to quantify the degree of contamination and determine the sensitivity to antimycotics. The cultivation procedure can take up to 7 days. The diagnostic sensitivity of the test reaches 90-95%. The duration of the culture study and the high cost limits the use of this method to individual clinical cases. The effectiveness of cultural methods is affected by the conditions of transportation of biological material and the preservation of the viability of the pathogen.

To detect DNA C. albicans and other species Candida in the Russian Federation, the PCR method is used with various options for detecting reaction products. Most commercially available kits of reagents are aimed at the qualitative detection of DNA C.albicans , which limits the application of the method. Currently, kits of reagents for the detection of DNA of the most common species of Candida : C. albicans , C.parapsilosis 9 have been developed and are commercially produced.0431 , C.tropicalis , C.glabrata , C.krusei using multiplex real-time PCR with quantitative evaluation of the results. These kits make it possible to carry out both species identification and assess the massiveness of colonization by fungi of the genus Candida . Diagnostic sensitivity in the diagnosis of vulvovaginal candidiasis ranges from 90 to 98%.

Indications for the use of various laboratory tests. Microscopic examination of the biomaterial is indicated in cases where patients have symptoms and clinical manifestations of an infectious and inflammatory process as the fastest method of etiological diagnosis. The study allows, along with the identification of laboratory signs of inflammation, to detect cells of yeast-like fungi.

A culture study is recommended for recurrent forms of infectious and inflammatory processes, when Candida are not detected microscopically and other potential pathogens of the pathological process (Trichomonas and other STI pathogens, pathogens of aerobic vaginitis) are excluded. Determining the degree of seeding increases the information content of the study. In the event of a recurrence of the inflammatory process against the background of antimycotic therapy, it is necessary to conduct a cultural study with species identification and determination of sensitivity to antimycotic drugs.

Since fungi of the genus Candida belong to saprophytes and can be present in low concentrations on the surface of the skin and mucous membranes, the use of only DNA detection for diagnosis (PCR, qualitative format) is not sufficiently informative. Determining the concentration of DNA Candida species albicans and non-albicans (real-time PCR, quantitative format) allows you to determine the degree of contamination and can be used in recurrent forms of infectious and inflammatory process to establish its etiology.

Features interpretation of laboratory results. Microscopic examination of blastospores and pseudomycelium of yeast-like fungi is diagnostic of candidiasis.