SEXUALLY TRANSMMITED DISEASES

PRESENTER: NYANGARA RAJABU FACILITATOR: ISAAC U. M DEPARTMENT OF

MICROBIOLOGY AND PARASITOLOGY

NEISSERIA
Genus: Neisseria Species: gonorrhoeae, meningitidis GENERAL CONCEPTS: Neisseria inhabit mucosal surfaces. There are 2 species that are pathogenic for humans: N. gonorrhoeae. Also referred to as the gonococcus, N. gonorrhoeae is responsible for the disease gonorrhea, named by Galen in the year 130 AD from the literal "flow of seed". N. meningitidis. Also referred to as the meningococcus, N. meningitidis is responsible for meningitis.

Gram-negative coccus, 0.6 to 1.0 m in diameter Usually seen in pairs with adjacent flattened sides. Outer membrane composed of proteins, phospholipids, and lipopolysaccharide. The organism is frequently found intracellularly in polymorphonuclear leukocytes (neutrophils) of the gonorrhea pustular exudate . Fimbriae, which play a major role in adherence, extend several micrometers from the cell surface Relatively fragile organism, susceptible to temperature changes, drying, uv light, and

Figure 1. Neisseria gonorrhoeae

Pathogenesis of Infection

Gonorrhea is a sexually transmitted disease. The sites of infection include the urethra (in men) and the cervix (in women). Fimbriae (pili) are very important for the gonococcus to attach to host cells A substance called Protein I makes up 66% of the outer membrane protein of N. gonorrhoeae. This protein is antigenic and is used as the basis of some serological tests. N. gonorrhoeae produce cytotoxic substances that damage ciliated epithelial cells in fallopian tubes; the LPS endotoxin may be partly responsible. N. gonorrhoeae also produce an extracellular protease that cleaves a proline-threonine bond in immunoglobulin IgA. This causes loss of antibody activity.

GONORRHEA

specific type of urethritis that practically always involves mucous membranes of the urethra, resulting in a copious discharge of pus *more apparent in the male than in the female *generally limited to superficial mucosal surfaces lined with columnar epithelium *most frequently involved are the urethra, cervix, rectum, pharynx, and conjunctiva. *gonorrhea in young girls may present as vulvovaginitis (NOTE Squamous epithelium, which lines the adult vagina, is not susceptible to infection by the N. gonorrhoeae. However, the prepubescent vaginal epithelium, which has not been keratinized under the influence of estrogen, may be infected) *Mucosal infections are usually characterized by a purulent discharge.

SIGNS AND SYMPTOMS

MALES most common symptom is a discharge: a scanty, clear or cloudy fluid OR may be copious and purulent Dysuria (difficulty in urination)is often present redness, swelling, heat, and pain in urethral tissues intense burning and pain upon urination asymptomatic: important reservoir for transmission; increased risk for developingcomplications

FEMALES *presents as endocervical infection in uncomplicated cases *vaginal discharge *dysuria *50% :asymptomatic.

COMPLICATIONS
MALE *prostatitis *orchitis FEMALES *salpingitis, with or without ovarian involvement (ovaritis) *pelvic inflammatory disease (PID).

DIAGNOSIS
Clinical: The symptoms of gonorrhea differ between the sexes. In men, a copious urethral exudate containing Gram- negative diplococci is common In women, disease is often asymptomatic.

Laboratory: Neisseria may be cultured on ThayerMartin agar or other suitable media with incubation in 10% CO2. Neisseria are strongly oxidasepositive, Gram-negative diplococci. N. gonorrhoeae oxidizes glucose only.

CONTROL
Sanitary: Condoms are useful for preventing gonorrhea. Chemotherapeutic: Penicillin is the drug of choice for treating gonorrhea. However, the number of resistant isolates continues to increase and other drugs must be employed in these cases.

NEISSERIA MENINGITIDIS

Identical in its staining and morphological characteristics to Neisseria gonorrhoeae Has a prominent antiphagocytic polysaccharide capsule; important virulence factor. Grouped on the basis of their capsular polysaccharides, into 12 serogroups Most important serogroups associated with disease in humans are A, B, C, Y, and W135. Requires peptone-blood base medium in a moist chamber containing 5-10% CO2 Extremely susceptible to temperatures above or below 37 degrees Undergo rapid autolysis after death, both in vitro and in vivo(NOTE: accounts for the dissemination of lipopolysaccharide or endotoxin during septicemia Colonize the posterior nasopharynx of humans Humans are the only known host.

PATHOGENESIS

Meningococci are spread via respiratory droplets, and transmission requires aspiration of infective particles Meningococci attach to the nonciliated columnar epithelial cells of the nasopharynx; attachment is mediated by fimbriae and other outer membrane components Invasion of the mucosal cells occurs by a mechanism similar to that observed with gonococci Bloodstream invasion; enters the central nervous system Bacteria undergoest autolysis during growth and released parts of their cell walls in a soluble form (NOTE: major toxc is lipooligosaccharide,LOS, and its mechanism is endotoxic; the other important virulence factor is the antiphagocytic polysaccharide capsule. Endotoxin, cytokines, and free radicals damage the vascular endothelium, producing platelet deposition and vasculitis.

NOTE: 3 important virulence factors: A polysaccharide capsule that enables the organism to resist phagocytosis A lipo-oligosaccharide endotoxin that can be shed in large amounts by a process called blebbing, causing fever, shock, and other pathophysiology An immunoglobulin A1 protease that cleaves lysosomal membrane glycoprotein-1 (LAMP1), helping the organism survive intracellularly

SIGNS AND SYMPTOMS

onset: abrupt or insidious fever and altered mental status the most consistent findings headache is an early, prominent complaint and is usually very severe nausea, vomiting, and photophobia are also common symptoms.

neurologic signs are common; convulsions or coma signs of meningeal irritation such as spinal rigidity, hamstring spasms and exaggerated reflexes

DIAGNOSIS:
Clinical: The symptoms of meningitis usually begin abruptly with headache and fever. However, confirmation of meningococcal infection requires bacteriologic culture. Laboratory: N. meningitidis oxidizes both glucose and maltose.

CONTROL
Sanitary Avoiding contact with infected persons can prevent meningitis. Immunological Only experimental vaccines are available. These vaccines target the meningococcal capsular polysaccharide but are not effective against group B (the most common isolate) because of its poor immunogenicity. Chemotherapeutic Penicillin is also the drug of choice for treating meningococcal meningitis.

Mycoplasma

Mycoplasma species are the smallest free-living organisms. size 0.2 - 0.8 m in diameter x 8 - 10 nm thick These organisms are unique among prokaryotes in that they lack a cell wall, a feature largely responsible for their biologic properties such as their lack of a reaction to Gram stain and their lack of susceptibility to many commonly prescribed antimicrobial agents, including beta-lactams. Mycoplasmal organisms are usually associated with mucosal surfaces, residing extracellularly in the respiratory and urogenital tracts. They rarely penetrate the submucosa, except in the case of immunosuppression or instrumentation, when they may invade the bloodstream and disseminate to different organs and tissues throughout the body.

4 types of organisms are responsible for most clinically significant infections that may come to the attention of practicing physicians. These species are Mycoplasma pneumoniae, Mycoplasma hominis, Mycoplasma genitalium, and Ureaplasma species.

Mycoplasma Hominis

Morphologically, the Mycoplasma appear as very small cocci (300 nm diameter). There are also elongated and filamentous forms. The organisms possess a protein attachment factor termed P1 that interacts with a specific cellular receptor and allows adherence to respiratory epithelium. On agar plates, Mycoplasma have a "fried egg" colonial morphology. The organisms have limited biosynthetic abilities; they require cholesterol for their cell membrane and can generate energy via the breakdown of arginine

Mycoplasma Hominis Symptoms

Painful Urination Infection in the urinary tract by Mycoplasma hominis often results in painful urination for men and women. This infection symptoms is common in most sexually transmitted diseases and can be mistaken for other STDs such as gonorrhea or chlamydia. Unusual discharge Men and women experience strange discharges a few weeks after contracting Mycoplasma hominis infections. This is because the extra mucus and infected fluids are being excreted by the body, resulting in these unusual--and often foul smelling-discharges. Pain during sex Women with a Mycoplasma hominis infection will often experience pain during intercourse. This is because the inflammation of the ureter presses upon the vaginal wall. When the vagina is engorged with blood from arousal, the two tissues press against each other. Penetration or sometimes just extreme excitement can result in painful sensations for women. Men do not typically feel pain during sex when infected with Mycoplasma hominis.

DIAGNOSIS
Clinical: Symptomology is equivocal and ambiguous; diagnosis is dependent on isolation. Laboratory: The bacteria can be grown using complex media with penicillin. A fluorescent antibody stain can be used to confirm the identification.

CONTROL
Sanitary: Avoidance of contacts, if possible. Immunological: No single vaccine is available. Natural resistance follows infection. Chemotherapeutic: Tetracycline or chloramphenicol are effective.

Shigella
Genus: Shigella Species: dysenteriae

GENERAL CONCEPTS Shigella dysenteriae is responsible for bacillary dysentery, a disease most often associated with crowded, unsanitary conditions. Other species of Shigella may produce milder forms of diarrheal disease.

DISTINCTIVE PROPERTIES

Shigellae are facultative, non-motile, Gram-negative bacilli. They possess the heat stable endotoxin (LPS) characteristic of Gram-negative bacteria. Shigellae are pathogenic primarily due to their ability to invade intestinal epithelial cells. S. dysenteriae also produces a heat labile exotoxin that is a neurotoxin acting upon the gray matter of the central nervous system.

PATHOGENESIS
Dysentery is an oral infection transmitted via fecal contamination of water or food. During the 1-4 day incubation period, penetration of bacteria into the mucosal epithelial cells of the intestine causes an intense irritation of the intestinal wall, producing cramps and a watery, bloody diarrhea

HOST DEFENSES
Unlike the salmonellae, shigellae are acid tolerant. As a consequence, gastric acidity provides little protection against infection. Protective defenses include the normal flora, secretory IgA and phagocytosis.

EPIDEMIOLOGY

Dysentery and other shigelloses occur worldwide but the hosts are limited to humans and primates. Because of their acid tolerance, relatively few organisms are required to produce disease. Indeed, as few as 10 cells can cause disease in 10% of healthy persons; 200 cells may cause disease in 40% of persons. Contaminated food and water are the primary sources for contracting dysentery, but person to person transmission may occur because of the low dose required to produce disease. About 60% of cases occur in children aged 1-10 years.

DIAGNOSIS
Clinical: As with other diarrheal diseases, clinical diagnosis alone is equivocal. Diarrhea, fever and a watery bright red blood tinged stool are classical symptoms, but isolation of the organisms is required for confirmation. Laboratory: Shigella can be readily isolated and characterized using standard bacteriologic media or rapid identification systems. Shigellae are non-motile, incapable of fermenting lactose and do not produce H2S. Serological techniques may be used for epidemiological characterization.

CONTROL
Sanitary: As with other fecal-oral diseases, dysentery is best prevented by assuring a safe water supply and proper disposal of feces. Chemotherapeutic: The use of antibiotics is debatable because the disease is self-limiting. If required, ampicillin or a trimethoprimsulphamethoxizole combination may be employed. Replacing lost fluids to prevent dehydration is most important for treating