Human Papillomavirus (hpv) Infection

The patient presenting genital warts in cauliflower shape leads me to a diagnosis of Human Papillomavirus (HPV) infection due to immunosuppression secondary to untreated past infection with Human Immunodeficiency Virus (HIV). This virus is the only recognized cause of this condition therefore a differential diagnosis with another condition like this one is not available.

1. What is the diagnosis?

The patient is diagnosed with giant condyloma of Buschke and Löwenstein (GCBL). According to MedScape, it is a slow-growing, locally destructive verrucous plaque that usually presents on the penis but may also occur elsewhere in the anogenital region. The symptoms fit best with this diagnosis which is secondary to infection with HIV making patient’s immunity susceptible and vulnerable against foreign pathogens such as HPV which causes GCBL. Also, lab results coincided with this diagnosis.

2. What are the common presenting signs and symptoms of GCBL?

GCBL starts as keratotic plaque which slowly expands into a cauliflower mass like our patient’s. Foul odor may be associated with ulcerations of the lesion on the penile area. Urethra can be enlarged as well. Regional lymphadenopathy such as the one on the inguinal area of the patient is evident due to secondary infection. Bleeding can also occur along with abscesses.

3. What are the risk factors and predisposing factors which promote HPV infection resulting in GCBL?

HPV causing GCBL is primarily transmitted via sexual contact with infected individuals. Those at risk are people with multiple sex partners that are not checked for STD infection. Also, people who don’t practice safe copulation are also at great risk. Most importantly, people with immunesuppression due to HIV infection like our patient are with greatest possibility of contracting the virus. If infected with the strain that causes GCBL, genital warts may occur long with other symptoms.

4. What is the pathophysiology of HPV?

HPV invades basal cells of the epidermis subsequently penetrating the skin and mucosa through abrasions in the genital area. After infection, a window period occurs for about 3 to 9 months. After which, virulence factors are intensified leading to the infection of host cells and development of atypical koilocytosis of genital warts. Though normally sexually transmitted, infected mother can also infect child at birth promoting respiratory lesions on newborn.

5. How does HPV promote the development of carcinoma?

The virus when remained in the body for years, coupled with immususceptibility, allows the conversion of normal cells to cancerous cells. This is called cervical intraepithelial neoplasia. This condition can progress into invasive cervical cancer among women. Women are at high risk of having cancer due to progression of HPV infected cells into cancer cells.

6. What are the immune evasion strategies used by HPV?

HPV evade immune-surveillance via virulence factors E6 and E7 proteins. These modulates cytokines and chemo-attractant expression, alter antigen presentation, and down-regulates IFN-pathways and adherence molecules. These mechanisms allow successful invasion of virus into the system. Also, they are opportunistic pathogens on people with HIV, as our patient, with their immune system being compromised.

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7. Why is that the disease is positive for HIV but negative in RPR?

RPR or rapid plasma reagin test is a test use to detect infection caused by bacteria Treponema pallidum, agent for STI syphilis. Unlike HIV that can cause immunosupression leading to potential HPV infection, reagin antibody is not likely to be detected among patients with HPV. Aside from they are different types of microbe, their coexistence is only applicable to those with seriously compromised immunity and with mixed infection. HIV antigen or antibody however can be detected because HPV infection is almost always secondary to HIV infection. Therefore, RPR can be negative whilst HIV be positive.