Urinary tract infections and sexually transmitted diseases

UTI sources

Autoinfection, fomites, opportunistic, STDs

Honeymoon cystitis

E. coli, Proteus spp, Enterobacteriaceae, Staphylococcus saprophyticus

Non-bacterial infections

Trichomonas vaginalis, Schistosoma hematobium

Descending infections

Bloodstream to kidneys, ureters and/or bladder: Salmonella spp, Staphylococcus aureus, Mycobacterium spp, Candida spp. Uncommon.

Iatrogenic UTIs

Urinary cathers #1 cause. Bacteria track up to bladder. Catheter disrupts cleansing action of urethra. Biofilms form on catheter surface. Organisms in biofilm have increased resistance to antibiotics.

Lower UTIs

Frequency, urgency. Dysuria: pain on urination. Pyuria. Bacteriuria. Catheterized cases may be asymptomatic. Bacterial prostatitis can exhibit generalized symptoms in addition (fever, lower back pain)


Infectious microorganisms are transmitted via exchange of body fluids from infected to susceptible partners. Effective mean for parasites to travel. No vector needed. No need to survive outside body. Victims are young and healthy. No dormant or quiescent stage needed. No need for complex life cycle or dramatic pathology. Organism can not be too virulent since victim must be outwardly healthy. Organisms must overcome powerful innate defenses. Must penetrate unbroken mucus membrane or otherwise attach to them and proliferate in a hostile environment

Hemophilus decreyi



Mycoplasma and Ureaplasma spp.

Candida alibicans

Fungal vaginitis & balanitis

Gardnerella vaginalis

Bacterial vaginosis

Cervical carcinoma

Linked to HPV infection

Prostate cancer

Risk correlates directly w/ lifetime number of sexual partners – agent unknown

Head and neck cancers

Correlates directly w/ ones lifetime number of oral sex partners – agent unknown

Neisseria gonorrhoeae

Gonococcal urethritis and vaginitis, PID, “Clap”, .... G- coccus. Aerobic. Oxidase+, non-sporeforming, sensitive to moderate heat and also to drying. Nutritionally fastidious. Grows on chocolate agar. Capneic: prefers 4-6% CO2 in atmosphere. Esp. true in fresh isolates from clinical materials.

N. gonorrhoeae virulence factors

IgA protease. LPS (causes TNF-alpha production). Anti-phagocytic capsule (effective in absence of Ig's). unusual pili (have antigenic variation by DNA rearrangement)

N. gonorrhoeae epidemiology

Obligate pathogen (fomites rare). Sexual transmission. No lower animal reservoirs. Asymptomatic carrier state exists (more common in females than males). Evolved to maximize transmission

N. gonorrhoeae pathogenesis

Seek columnar cells of distal urethra or cervix. Anchor to these cells via pili and outer proteins. For biofilm. Organism multiplies in situ. Large number of virulent cells shed into genital secretions. Gonococci spread upward into urethra or cervix (urethral and cervical contractions may contribute because N. gonorrhoeae have no flagella. Usually limited to urethra in males. Can reach fallopian. Bloodstream infections in those who lack complement. Chronic infection in either sex can produce scarring and stricture of fallopian tubes or urethra, with severe effects

Gonococcal cervicitis

Often asymptomatic. Else: Cervical discharge, vaginal bleeding, abdominal pain

Gonococcal Chronic infection.

Female: Chronic pelvic pain, ectopic pregnancy, scarring & stricture of fallopian tubes, recurrent secondary infections. In males: scarring and stricture of the urethra

Purulent urethritis

Males. Copius flow of yellowish pus from urethra. Pain, often intense, on urination. Extreme difficulty in urination.

Disseminated gonococcal infections

Highest incidence in females. Pustular exanthem (can be sparse). Inflammation of tendons and/or joints (can become suppurative arthritis). Symptoms of sepsis: fever toxicity

N. gonorrhoeae presumptive diagnosis

Clinical signs and symptoms. Microscopic examination of Gram stained clinical material (cervical swab and urethral discharge). Must see G- diplococci contained w/in pus cells.

N. gonorrhoeae definitive diagnosis

Must do culture on chocolate or Thayer-Martin (VCN) agar to retard background flora. Must show that organism is N. gonorrhoeae. Fermentation of sugars, serotyping, ligase chain reaction rapid test still in development. Must determine antimicrobial susceptibility

N. gonorrhoeae treatment

Ceftriaxone. Single dose oral therapy.

N. gonorrhoeae prevention

No vaccine. Condom. Case finding/ partner notification. Intravaginal microbiocide releasing device

Chlamydia spp.

Obligate intracellular parasites. No muramic acid in cell wall. Stain blue w/ Giemsa. Generally parasatize epithelial cells.

C. trachomatis

Human pathogen. No reservoirs. Serotypes A-L. Serotypes A-C cause trachoma. Serotypes D through K cause STDs (cervicitis, proctitis, conjunctivitis, neonatal pneumonia). Serotypes L1 through L3 cause lymphogranuloma venereum.

C. psittaci

Natural host is brids (mainly psittacines). Zoonoses. Psitacossis (parrot fever). Pneumonia-like disease marked by fever, non-productive cough, diffuse infiltration in lower lungs, slow recovery. Contracted by inhalation of dust from bird feces. Organism is carried in GI tract of birds. Releassed mainly by sick or stressed birds.

C. pneumoniae

Human. No reservoirs. Causes pneumonia. Linked to arthritis, atherosclerosis, alzheimer's.

C. trachomatis epidemiology

50-70% of infections in women are silent. Unrecognized and untreated, the bacteria may remain infectious in the host for months and be readily transmitted to sex partners. Main age: 15-24. young women w/ cervical chlamydial infections are at heightened risk for pelvic inflammatory disease. Long-term reproductive sequelae such as pelvic pain, ectopic pregnancy, tubal infertility. Babies born to infected mothers are also at risk for conjunctivitis and/or pneumonia.

C. trachomatis pathogenesis

Elementary body is transmissible. Parasite induced endocytosis. EB --> reticulate body. Progeny are in the form of EBs that can infect other cells. Serotypes D-K have binding preference for epithelial cells. Immune response is important for pathogenesis (immune system responsible for many overt symptoms).

Elementary body

Extracellular form. Sub-microscopic, only 0.2u in diameter. Cryptobiotic: no active metabolism. Receptor mediated endocytosis. Maintains pH above 6.2 & prevents fusion w/ lysosomes

Reticulate body

Metabolically active form. 4X larger than EB. Uses energy from host cell. Hollow tubes protruding from membrane allows for nutritional intake while still within vacuole. Can not survive outside host cell

C. trachomatis diagnosis

Multiple infections possible (gonnococcal and Chlamydial infection) . Isolation and culture (Gold Standard). Many false negatives. Microscopic detection. ELISA, PCR and LCR

Ur-Sure PLUS

Use urine of urethral swab to test for Neisseria and Chlamydia infections. Uses TMA (transcripiton mediated amplification). Proprietary process. Amplifies and identifies rRNA from either Neisseria gonorrhea or Chlamydia trachomatis. Screening only (confirmatory test required)

C. trachomatis treatment

EB particles are resistant to drugs. Treatment must be given for a long time (Chlamydia are slow growing). Tetracycline, erythromycin, sulfonamide, azithomycin


Enhanced tissue penetration, long-term persistence in tissue, effective in one or two doses.

Treponema sp.

Slim, stright

Leptospira sp.

Slim, curved

Borrellia sp

Thick, irregular


Found in spirochetes. Fibrils originate at end of cells and run along the side of the cylindrical cell past the center. Fibrils originate at each end of the cell; therefore, some of them cross in the middle. Fibrils are wound around the cylinder and are capable of motion

Treponema pallidum

Venereal syphilis. PH 7.2-7.4. 30-37C, O2 1-4%. eH: -230 to -240mV. Worldwide, adults. Can be congenital. Incubation 10-90 days. All tissues affected. Destructive, highly invasive w/ perivascular cuffing. Transmission exclusively by exchange of body fluids. No fomite vector. All lab diagnosis must be serologic (except dark field microscopy of chancre).


Treponema pertinue. Frambesia. Hot, wet climates. Children skin (& bone) infection. No congenital form. 14-28 day incubation. Destructive & somewhat invasive


Treponema carateum. Carate. Hot, wet areas in the Americas. Older children. Skin infection. 2-6 month incubation. Not destructive, little invasion & perivascular cuffing

Endemic syphilis

Treponema endemicum. Bejel. Hot, dry areas of Africa. All ages affected. Infects mucus membranes and can be found there and the skin. Destructive and somewhat invasive w/ perivascular cuffing


Spreading factor for T. pallidum. Penetrates tissue ground substance


Inhibits complement activation against T. pallidum.

Sialic acid

Complement inhibitor found in T. pallidum

Prostaglandin E-2

Inhibits immune function. Found in T. pallidum

Primary syphilis

Hard, painless chancre at point of contact. Disappears within 1 week after proper treatment. Disappears spontaneously without treatment after 4-12 weeks. Greyish mass covering crater filled w/ T. pallidum cells. Diagnosis by darkfield microscopy: examine exudate form lesion


Found in primary syphilis. Fluid filled lesion that is painless. Full of bacteria. Often found in vaginal wall or uterine cervix thus escaping notice.

Secondary syphilis

Starts from 6 weeks to months after infection. Rarely concurrent w/ chancre. 80% of those w/ secondary infection show the maculopapular rash. Rash may extend to cover the face, palms and soles. Condylomata (large lesions) at mucocutaneous junctions common around anus and labia. Patient is almost always seropositive.

Latent stage of syphilis

Absence of symptoms, but patient is seropositive. Quiescent treponemes somewhere in the body. Early latent lasts for 2 years or less. Relapse to secondary symptoms may occur. During these the patient is infectious. Late latent: no relapses, non infectious. May last life time of patient or may progress to tertiary syphilis

Tertiary syphilis

Late benign gummatous. Hypersensitive granulomatous reaction. Destructive to viscera or mucocutaneous areas. Cardiovascular: weakening of the vessels of the heart. Ends in an aneurism. Prognonsis is death.


Early and late. Part of tertiary syphilis. Early is found in AIDS patients. Late: causes “dementia praecox”, paresis, and tabes dorsalis (loss of dorsal columns). Loss of position sensation. Charcot's joint: trauma to knee and ankle. Argyll robertson pupil. Pupil only reacts to light when it is moved from far to near. Dementia.

Congenital syphilis

Crosses placental and uterine membranes. Mostly occurs in spontaneous and septic abortion. Teratogenic effects can be seen in live borns. Stigmata: rash of secondary syphilis, saber shins, snuffles, pronounced maxilla, hutchinson's teeth (translucent, pegged and notched).

Treponemal tests

Use cells to T. pallidum as antigen and patient serum as source for antibody. TPI, RPCf, FTA-Abs, TPHA or HAT, and MHAT

Non-treponemal tests

Use alternative to bacteria as antigen, but still use patient serum as antibody. Cardiolipin, VDRL give many false positives. HIV can give false negatives because cardiolipiin is elevated to such a degree that a prozone phenomenon occurs: VDRL, RPR reactions inhibited

Reaginic antibodies

2 definitions. Antibodies causing a type I immediate hypersensitivity reaction (now known as IgE). Antibodies of the IgM class produced by persons w/ Treponema spp infections. This Ab does not bind any known treponemal antigens.

Syphilitic reagins

Antibodies of the IgM class. Non-specifically react w/ a variety of tissue phospholipids. In theory, these lipids are normally hidden from the immune system and are released only by microbial damage during some infections.

Schleppering agent

Enhances antigenicity of the lipids for syphilitic reagins. Normally found in serum


Commercially prepared as an alcoholic extract beef heards. Lechithin is added to neutralize anti-complement properties and cholesterol is added to increase reactive surface and boost complement fixing ability. Antigen in non-trepenemal tests. All give many false positives.

Prozone phenomenon

Inhibits reactions due to excessively high concentrations. Dillution is required for testing to be meaningful.

MHAT test

8 samples X 12 dilutions. Wells which are positive for an agglutination reaction show diffuse coloration. Wells which are negative show a red dot in the center.

Syphilis treatment

Primary and secondary respond well. Latent and tertiary stages do not respond to treatment. Penicillin and derivatives are drug of choice. Significant drug resistance has not yet appeared in this organism.


Bacterial meningitis

Often acute, life threatening

Chronic meningitis

Insidious , insidious progressive over weeks (TB, Fungi, protozoa). Rare.

Aseptic/viral meningitis

Usually self-limiting


Inflammation of the brain tissue. Most often viral. May not show signs compatible w/ aseptic meningitis, but have clinical features of CNS infection. Meningoencephalitis (signs of both)

Meningitis pathology

Blood stream (bacteremia/viremia) --> seeding of meninges

Neonatal bacterial meningitis

Group B Streptococcus. Less common E. coli, Listeria monocytogenes. < 1 year of age. Immature immune system. Increased risk w/ PROM, prematurity, long term effects, difficult diagnosis. Often very general signs and symptoms.

Bacterial meningitis in children

Infants and children w/ no underlying abnormalities are prone to get: S. pneumoniae, N. meningitidis. Less common: Haemophilus influenza Type B

Bacterial meningitis in adults

S. pneumoniae, N. meningitidis. Less common: Listeria monocytogenes.

Group B streptococcus

20-30% women have vaginal infection. Prenatal screening required for this reason. Capsular antigens and lack of antibodies play role in virulence. Early onset during birth, late onset from nursery play.

E. coli

Rare cause of neonatal meningitis. Acquired during vaginal delivery. Virulence: adherence (fimbriae), polysaccharide capsule (phagocytosis).

Listeria monocytogenes in infants

G+ bacillus w/ range of shapes and sizes. Environmental sources include some foods (soft cheeses, processed meat), intrauterine infections (transplacental transmission following maternal bacteremia). Risk of neonatal disease in vaginally colonized mothers.

Listeria monocytogenes in adults

Sporadic cases in those w/ immune compromise (t cell defects, transplants and others on steroids, cancers (lymphoma))

Haemophilus influenzae B

Was most common cause of childhood meningitis until vaccine was available. Pleomorphic G- bacilli. Vaccine started at 2 months. Essentially eliminated invasive HIB disease.

S. pneumoniae

G+ cocci in short chains. Virulence: large polysaccharide capsule; many capsular types; vaccine provided to adults (>65) and high risk individuals / children eg asplenia (23 capsular types). Sporadic cause of meningitis in children and adults. Sporadic cause of meningitis

N. meningitidis

G- diplococci. Often intracellular. Most common cause of bacterial meningitis. Young adults and children. Sporadic v. endemic. Occasional outbreaks schools, colleges, military. 500,000 cases worldwide w/ 50,000 deaths. Petechial rash in many (diagnosis). Vaccine in outbreaks. Antibiotics for direct contact. 20-30% carry in nasopharynx. What allows it to become an invasive pathogen? Largely unknown. Complement deficiency, antibody deficiency (never encountered that strain). Fimbriae, polysaccharide capsule. Capsular type C most common in outbreaks.

Meningococcal vaccine

Quadrivalent: A, C, Y, W-135. B is missing! Duration of immunity is unknown, but believed to be > 3 years for those > 4. revaccination after 2-3 years for children at high risk. Use in outbreaks and travel to endemic areas (subsaharan Africa).

Blood culture

Must obtain blood culture since organism must enter blood to get to meninges. CSF: protein and glucose, cell count and differental. Gram stain and Bacterial culture.

CSF parameters in bacterial meningitis

Glucose decreases, protein increases. White cells increased thousands / mm3. White cell count differential: predominantly neutrophils (polymorphonuclear neutrophils). Gram stain findings (may find bacteria, or there may be a low volume and they may not be observed).

Cryptococcus neoformans

Yeast w/ large capsule. India in. causes meningitis or meningoencephalitis. Most common in T-cell deficiency (lymphoma, AIDS, steroids). Infection is less aggressive then bacterial meningitis. Prolonged therapy needed. Eradication in AIDS patient is difficult to impossible. Life long therapy required.

Diagnosis of C. neoformans

India ink if nothing else possible (not sensitive). Gram stain (also lacks sensitivity). Culture 24-48 hours. Latex agglutination.

Latex agglutination

Latex beads coated w/ antibody specific to C. neoformans. Add to CSF; if C. neoformans present, visible agglutination occurs. Can be used to monitor therapy


SsRNA viruses. Coxsacie A, B; echo virus; poliovirus (3 serotypes). Feco-oral transmission. Water sources Summer/fall to winter in tropics. Array of diseases depends on serotype and tissue tropism. 60% asymptomatic/subclinical. CNS infection usually meningitis (self limiting) but occasionally encephalitis w/ permanent damage


Major cause of disease in developing countries due to lack of vaccine distribution. CNS tropism. Motor neuron cells targeted and destroyed. Most infections asymptomatic. Paralytic poliomyelitis most serious manifestation. (asymmetrical flacid paralysis).

Polio vaccine

Inactivated polio virus. Oral polio: best overall; herd immunity: virus shed in stool; 1 /2.6 million doses = vaccine associated paralytic polio; storage temperature dependent

CSF parameters in viral meningitis

Protein & glucose occasionally altered. WBC increased, but not as much as in bacterial meningitis (100's to 1000's). predominantly lymphocytes. Grame stain show nothing.

Diagnosis of viral meningitis

Virus culture (+ in 50% of cases). PCR**, often unconfirmed


Fever, headache, and behavioral changes, altered level of consciousness. Most common viruses: herpes simplex, varicella zoster, arboviruses


Japenese, Eastern, Western, St. Louis, California encephalitis, West Nile. Vector born. Natural host is birds.

Herpes encephalitis

DsDNA (latent virus) most common cause. HSV-1. Trigeminal nerve root ganglion w/ extension to temporal lobe. Usually one lobe = focal neurologic signs. Classic changes on EEG. 70% mortality if untreated. Treatment: acyclovir, famciclovir. 20% mortality if treated. 50% of survivors have permanent neural damage

West nile virus

Closely related to St. Louis encephalitis. Genetically linked to middle eastern strain. Seasonal incidence (mosquito population).


10% develop CNS infection of which some may develop encephalitis.


Antivirals are somewhat effective. 1/2000 individuals infected develop encephalitis -> 15% mortality (100% in immunosuppressed)


1/1000 infected develop encephalitis w/ 40% mortality. SSPE (subacute sclerosing panencephalitis). Chronic CNS infection: 1/100,000; symptoms may occur 2-6 years post infection.

Diagnosis of encephalitis

Clinical criteria; virus isolation in CSF; PCR best test; antibody detection (4-fold increase in acute vs. convalescence); high single titer; IgM (not always an IgM test and non-specific)

Rare causes of encephalitis

HHV-6, EBV, CMV, adenovirus, rabies


Main reservoirs: racoons, skunks, foxes, bats. > 90% of human rabies from dogs. Inocculation w/ bite --> uptake to CNS via peripheral nerves. Incubation of days to months w/ ave of 1-3 months (size of inoculum and site of infection). Active cerebellar infection and local spread. Cytoplasmic eosinophilic inclusion bodies in neuronal cells

Negri bodies

Cytoplasmic inclusion bodies found in neurons of those w/ rabies. Can be used for post-mortem diagnosis.

Rabies diagnosis in animals

Brain sampling and direct fluorescent antibody tests

Rabies diagnosis in humans

Saliva: PCR; antibody (blood and CSF), skin biopsy for antigen in cutaneous nerves. Usually > 1 test done to rapidly confirm disease.

Rabies treatment

Post exposure prophylaxis. Immune globulin. 5 doses over 28 days of rabies vaccine. (intramuscular)

Bovie spongiform encephalitis

Transmissible bovine encephalopathy. Mad cow disease. Degenerative fatal brain disorder primarily in UK (France, Ireland, Spain). Not bacterial, so gram staining reveals nothing


Creutzfield-Jakob disease. Prion disease including BSE. It is the manifestation of mad cow disease in man. nvCJD has slower expression.


Variant CJD. Ruminant tissues rendered to make feed. Feed given to calves. CNS tissue in feed. Epidemic stopped by removing CNS tissue from feed processing. 122 deaths + 130 known to have disease.

Diagnosis of CJD

Brain biopsy on absolute diagnosis. Spongiform encephalopathy. Sporadic usually post mortem. No cells in CSF, proteins: 14-3-3

Brain abscess

Localized collection of pus in the brain tissue.

Brain abscess etiology

Result of direct trauma or inoculation during surgery (S. aureus, Strep, anaerobes). Hematogenous spread following other infections (staph and strep). Direct extension from ears and sinuses (anaerobes and respiratory pathogens)

Diagnosis of brain abscess

CT or MRI. Treatment is surgery and antibiotic therapy to cover broad spectrum of organisms including Gram positive, gram negative and anaerobes

Listeria monocytogenes

Gram positive pleomorphic bacilli: coccobacilli

Meningococcal petechial rash

Gram stain of rash. Break and touch directly w/ a microscopic slide. Observe for G- diplococci (Neiserria)

Haemophilus influenza

Small G- bacilli

Progressive multifocal leucoencephalopathy

PML. A disease caused by a typical agent. Parvovirus

Subacute schlerosing parencephalitis

SSPE. Measles virus. Typical agent.

Progressive encephalitis

Rubella. Progressive neurological impairment including dementia, ataxia, spasticity, and occasional myoclonus


Stellite RNA. Circular, 100s of nucleotides in length. Mostly foundin plants, require helper virus. HDV. Adeno-associated virus


Closed circular, naked ssRNA causing infections in plants


Infectious proteins that have no Nucleic acid or protein capsid.


Infectious proteins that have no Nucleic acid or protein capsid.

Transmissible encephalopathy

No nucleic acids. Resistant to UV, EtOH, boiliing, formalin, 10% B-propiolactone, nucleases. Can be inactivated by acetone and ether. Replicates in high titer in susceptible tissue, no pathologic evidence of an inflammatory process. Fatal CNS disorders. Interferon useless. Transmissible to experimental animals.

Prions in humans

Kuru, Gerstman-Straussler disease, Creutzfeld-Jakob disease, mad cow disease

Prion pathology

Abnormal astrocyte proliferation, confined to CNS, depletion of dendritic spines in neurons w/ vacuolization of cells, fibrillar amyloid (reacts w/ congo red). Spongy brain

Scrapie etiology

Sheeps! Accumulation of an abnormal isoform of a membrane glycoprotein normally present in all people. Normal or abnormal PrP transconformation of protein PrPC

Prion protein cellular

PrPC. Isolated protein theory. PrPC is modified to PrPSc (scrapie) which accumulates (fibrillar amyloidosis). 33-35 kDa in weight. Sensitive to proteinase K. ubiquitous in the body, but cerebral concentrations are highs. Familial forms are secondary to a PRNP gene mutation. Family forms are genetically transmissible but not contagious.


Numerous outbreaks


BDV. Bornaviridae. ss(-)RNA, non-segmented. Progressive encephalopathy in horses.diagnosis by Specific antibody test. Causes ataxis, nystagmus, paralysis, drowsiness, reduced visual acuity, anorexia. Highly neurotropic. Probably gains access to CNS via intraaxonal migration through olfactory nerve or nerve endings in the oropharyngeal and intestinal regions. T-cell mediated pathogenesis demonstrated. Higher occurance in psychiatric patients.

Equine morbillivirus

Hendra virus. Deadly to humans, horses, cats, guinea pigs. Harmless in bats (natural host). Requires P4 facility for handling

Nipah virus

Paramyxoviridae. Viral encephalitis epidemic in the pig farm workers. Similar to hendra virus. Porcine respiratory and encephalitis syndrome or barking pig syndrome.


Reoviridae. Tick borne: Dermacentor andersonii. Flu-like. Meningoencephalitis; stiff neck, headache. Marked thrombocytopenia, pleocytosis (lymphocytes, elevated protein). Diagnosis by isolation from culture of serum. Isolation can be conducted by intracerebral injection in neonatal mice. Indirect immnunofluorescence, RT-PCR amplification on one or several genome segments enables diagnosis at an early phase.

Encephalitis lethargic

Von Economo's disease. 60% mortality. Symptoms: progressive onset of weariness, headache, weight loss, bouts of hiccups, fever. Many nervous disorders. Occasional cases.