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13 terms

Week 6 Microbes and Viruses

STUDY
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Treponema
Disease
Syphilis.

Characteristics
Spirochetes. Not seen on Gram-stained smear because organism is too thin. Not cultured in vitro.

Habitat and Transmission
Habitat is the human genital tract. Transmission is by sexual contact and from mother to fetus across the placenta.

Pathogenesis
Organism multiplies at site of inoculation and then spreads widely via the bloodstream. Many features of syphilis are attributed to blood vessel involvement causing vasculitis. Primary (chancre) and secondary lesions heal spontaneously. Tertiary lesions consist of gummas (granulomas in bone, muscle, and skin), aortitis, or central nervous system inflammation. No toxins or virulence factors known.

Laboratory Diagnosis
Seen by darkfield microscopy or immunofluorescence. Serologic tests important: VDRL (or RPR) is nontreponemal (nonspecific) test used for screening; FTA-ABS is the most widely used specific test for Treponema pallidum. Antigen in VDRL is beef heart cardiolipin; antigen in FTA-ABS is killed T. pallidum. VDRL declines with treatment, whereas FTA-ABS remains positive for life.

Treatment
Penicillin is effective in the treatment of all stages of syphilis. In primary and secondary syphilis, use benzathine penicillin G (a depot preparation) because T. pallidum grows slowly, so drug must be present for a long time. There is no resistance.

Prevention
Benzathine penicillin given to contacts. No vaccine is available.
Neisseria gonorrhoeae
Disease
Gonorrhea. Also neonatal conjunctivitis and pelvic inflammatory disease.

Characteristics
Gram-negative "kidney-bean" diplococci. Oxidase-positive. Insignificant capsule.

Habitat and Transmission
Habitat is the human genital tract. Transmission in adults is by sexual contact. Transmission to neonates is during birth.

Pathogenesis
Organism invades mucous membranes and causes inflammation. Endotoxin present but weaker than that of meningococcus, so less severe disease when bacteremia occurs. No exotoxins identified. IgA protease and pili are virulence factors.

Laboratory Diagnosis
Gram-stained smear and culture. Organism visible intracellularly within neutrophils in urethral exudate. Oxidase-positive colonies on Thayer-Martin medium. Gonococci do not ferment maltose, whereas meningococci do. Serologic tests not useful.

Treatment
Ceftriaxone for uncomplicated cases. Tetracycline added for urethritis caused by Chlamydia trachomatis. High-level resistance to penicillin is caused by plasmid-encoded penicillinase. Low-level resistance to penicillin is caused by reduced permeability and altered binding proteins.

Prevention
No drug or vaccine. Condoms offer protection. Trace contacts and treat to interrupt transmission. Treat eyes of newborns with erythromycin ointment or silver nitrate to prevent conjunctivitis.
N. meningitidis
Diseases
Meningitis and meningococcemia.

Characteristics
Gram-negative "kidney-bean" diplococci. Oxidase-positive. Large polysaccharide capsule. One of the three classic encapsulated pyogenic bacteria (Streptococcus pneumoniae and Haemophilus influenzae are the other two).

Habitat and Transmission
Habitat is the human upper respiratory tract; transmission is via respiratory droplets.

Pathogenesis
After colonizing the upper respiratory tract, the organism reaches the meninges via the bloodstream. Endotoxin in cell wall causes symptoms of septic shock seen in meningococcemia. No known exotoxins; IgA protease produced. Capsule is antiphagocytic. Deficiency in late complement components predisposes to recurrent meningococcal infections.

Laboratory Diagnosis
Gram-stained smear and culture. Oxidase-positive colonies on chocolate agar. Ferments maltose in contrast to gonococci, which do not. Serologic tests not useful.

Treatment
Penicillin G (no significant resistance).

Prevention
Vaccine contains capsular polysaccharide of strains A, C, Y, and W-135. One form of the vaccine contains the polysaccharides coupled to a carrier protein (diphtheria toxoid) and one contains only the polysaccharides. Rifampin or ciprofloxacin given to close contacts to decrease oropharyngeal carriage.
Chlamydia trachomatis
Diseases
Nongonococcal urethritis, cervicitis, inclusion conjunctivitis, lymphogranuloma venereum, and trachoma. Also pneumonia in infants.

Characteristics
Obligate intracellular parasites. Not seen on Gram-stained smear. Exists as inactive elementary body extracellularly and as metabolically active, dividing reticulate body intracellularly.

Habitat and Transmission
Habitat is the human genital tract and eyes. Transmission is by sexual contact and during passage of neonate through birth canal. Transmission in trachoma is chiefly by hand-to-eye contact.

Pathogenesis
No toxins or virulence factors known.

Laboratory Diagnosis
Cytoplasmic inclusions seen on Giemsa-stained or fluorescent antibody-stained smear. Glycogen-filled cytoplasmic inclusions can be visualized with iodine. Organism grows in cell culture and embryonated eggs, but these are not often used. PCR-based assay and an ELISA using patient's urine are available.

Treatment
A tetracycline (such as doxycycline) or a macrolide (such as azithromycin).

Prevention
Erythromycin effective in infected mother to prevent neonatal disease. No vaccine is available.
Herpes Type 1
Diseases
Herpes labialis (fever blisters or cold sores), keratitis, encephalitis.

Characteristics
Enveloped virus with icosahedral nucleocapsid and linear double-stranded DNA. No virion polymerase. One serotype; cross-reaction with HSV-2 occurs. No herpes group-specific antigen.

Transmission
By saliva or direct contact with virus from the vesicle.

Pathogenesis
Initial vesicular lesions occur in the mouth or on the face. The virus then travels up the axon and becomes latent in sensory (trigeminal) ganglia. Recurrences occur in skin innervated by affected sensory nerve and are induced by fever, sunlight, stress, etc. Dissemination to internal organs occurs in patients with depressed cell-mediated immunity with life-threatening consequences. HSV-1 encephalitis often affects the temporal lobe.

Laboratory Diagnosis
Virus causes cytopathic effect (CPE) in cell culture. It is identified by antibody neutralization or fluorescent antibody test. Tzanck smear of cells from the base of the vesicle reveals multinucleated giant cells with intranuclear inclusions. These giant cells are not specific for HSV-1; they are seen in the vesicular lesions caused by HSV-2 and varicella-zoster virus as well. A rise in antibody titer can be used to diagnose a primary infection but not recurrences. HSV encephalitis can be diagnosed using a PCR assay to detect HSV-1 DNA in spinal fluid.

Treatment
Acyclovir for encephalitis and disseminated disease. Acyclovir has no effect on the latent state of the virus. Trifluorothymidine for keratitis. Primary infections and localized recurrences are self-limited.

Prevention
Recurrences can be prevented by avoiding the specific inciting agent such as intense sunlight. Acyclovir can reduce recurrences. No vaccine is available.
Herpes Type 2
Diseases
Herpes genitalis, aseptic meningitis, and neonatal infection.

Characteristics
Enveloped virus with icosahedral nucleocapsid and linear double-stranded DNA. No virion polymerase. One serotype; cross-reaction with HSV-1 occurs. No herpes group-specific antigen.

Transmission
Sexual contact in adults and during passage through the birth canal in neonates.

Pathogenesis
Initial vesicular lesions occur on genitals. The virus then travels up the axon and becomes latent in sensory (lumbar or sacral) ganglion cells. Recurrences are less severe than the primary infection. HSV-2 infections in neonate can be life-threatening because neonates have reduced cell-mediated immunity. Asymptomatic shedding of HSV-2 in the female genital tract is an important contributing factor to neonatal infections.

Laboratory Diagnosis
Virus causes CPE in cell culture. Identify by antibody neutralization or fluorescent antibody test. Tzanck smear reveals multinucleated giant cells but is not specific for HSV-2. A rise in antibody titer can be used to diagnose a primary infection but not recurrences.

Treatment
Acyclovir is useful in the treatment of primary and recurrent genital infections as well as neonatal infections. It has no effect on the latent state.

Prevention
Primary disease can be prevented by protection from exposure to vesicular lesions. Recurrences can be reduced by the long-term use of oral acyclovir. Neonatal infection can be prevented by delivering the child by cesarean section if the mother has visible vesicular lesions in the birth canal. There is no vaccine.
HIV
Disease
Acquired immunodeficiency syndrome (AIDS).

Characteristics
Enveloped virus with two copies (diploid) of a single-stranded, positive-polarity RNA genome. RNA-dependent DNA polymerase (reverse transcriptase) makes a DNA copy of the genome, which integrates into host cell DNA. Precursor polypeptides must be cleaved by virus-encoded protease to produce functional viral proteins. The tat gene encodes a protein that activates viral transcription. Antigenicity of the gp120 protein changes rapidly; therefore, there are many serotypes.

Transmission
Transfer of body fluids, e.g., blood and semen. Also transplacental and perinatal transmission.

Pathogenesis
Two receptors are required for HIV to enter cells. One receptor is CD4 protein found primarily on helper T cells. HIV infects and kills helper T cells, which predisposes to opportunistic infections. Other cells bearing CD4 proteins on the surface, e.g., astrocytes, are infected also. The other receptor for HIV is a chemokine receptor such as CCR5. The NEF protein is an important virulence factor. It reduces class I MHC protein synthesis, thereby reducing the ability of cytotoxic T cells to kill HIV-infected cells. Cytotoxic T cells are the main host defense against HIV.

Laboratory Diagnosis
HIV can be isolated from blood or semen, but this procedure is not routinely available. Diagnosis is usually made by detecting antibody with ELISA as screening test and Western blot as confirmatory test. Determine the "viral load," i.e., the amount of HIV RNA in the plasma, using PCR-based assays. A high viral load predicts a more rapid progression to AIDS than a low viral load. PCR-based assays can also detect viral RNA in infected cells, which is useful to detect early infections before antibody is detectable.

Treatment
Nucleoside analogues, such as zidovudine (AZT), lamivudine (3TC), stavudine (d4T), didanosine (ddI), and zalcitabine (ddC), inhibit HIV replication by inhibiting reverse transcriptase. Nonnucleoside inhibitors of reverse transcriptase, such as nevirapine and efavirenz, are used also. Protease inhibitors, e.g., indinavir, ritonavir, and saquinavir, prevent cleavage of precursor polypeptides. Highly active antiretroviral therapy (HAART) consists of two nucleoside inhibitors and one protease inhibitor. Clinical improvement occurs, but the virus persists. Enfuvirtide, a "fusion inhibitor," which blocks entry of HIV, and maraviroc, which inhibits binding of the gp120 envelope protein of HIV to the cell co-receptor CCR-5, are also useful. Treatment of the opportunistic infection depends on the organism.

Prevention
Screening of blood prior to transfusion for the presence of antibody. "Safe sex," including the use of condoms. AZT with or without a protease inhibitor should be given to HIV-infected mothers and their newborns. Zidovudine (AZT), lamivudine (3TC), and a protease inhibitor should be given after a needle-stick injury. There is no vaccine.
Varicella-Zoster Virus
Diseases
Varicella (chickenpox) in children and zoster (shingles) in adults.

Characteristics
Enveloped virus with icosahedral nucleocapsid and linear double-stranded DNA. No virion polymerase. One serotype.

Transmission
Varicella is transmitted primarily by respiratory droplets. Zoster is not transmitted; it is caused by a reactivation of latent virus.

Pathogenesis
Initial infection is in the oropharynx. It spreads via the blood to the internal organs such as the liver and then to the skin. After the acute episode of varicella, the virus remains latent in the sensory ganglia and can reactivate to cause zoster years later, especially in older and immunocompromised individuals.

Laboratory Diagnosis
Virus causes CPE in cell culture and can be identified by fluorescent antibody test. Multinucleated giant cells seen in smears from the base of the vesicle. Intranuclear inclusions seen in infected cells. A fourfold or greater rise in antibody titer in convalescent-phase serum is diagnostic.

Treatment
No antiviral therapy is indicated for varicella or zoster in the immunocompetent patient. In the immunocompromised patient, acyclovir can prevent dissemination.

Prevention
Both the varicella vaccine and the zoster vaccine contain live, attenuated varicella-zoster virus. Immunocompromised patients exposed to the virus should receive passive immunization with varicella-zoster immune globulin (VZIG) and acyclovir to prevent disseminated disease.
Cytomegalovirus
Diseases
Most common cause of congenital abnormalities in the United States. Cytomegalic inclusion body disease in infants. Mononucleosis in transfusion recipients. Pneumonia and hepatitis in immunocompromised patients. Retinitis and enteritis, especially in AIDS patients.

Characteristics
Enveloped virus with icosahedral nucleocapsid and linear double-stranded DNA. No virion polymerase. One serotype.

Transmission
Virus is found in many human body fluids, including blood, saliva, semen, cervical mucus, breast milk, and urine. It is transmitted via these fluids, across the placenta, or by organ transplantation.

Pathogenesis
Initial infection usually in the oropharynx. In fetal infections, the virus spreads to many organs, e.g., central nervous system and kidneys. In adults, lymphocytes are frequently involved. A latent state occurs in leukocytes. Disseminated infection in immunocompromised patients can result from either a primary infection or reactivation of a latent infection.

Laboratory Diagnosis
The virus causes CPE in cell culture and can be identified by fluorescent antibody test. "Owl's eye" nuclear inclusions are seen. A fourfold or greater rise in antibody titer in convalescent-phase serum is diagnostic.

Treatment
Ganciclovir is beneficial in treating pneumonia and retinitis. Acyclovir is ineffective.

Prevention
No vaccine is available. Ganciclovir suppresses retinitis. Do not transfuse CMV antibody-positive blood into newborns or antibody-negative immunocompromised patients.
Epstein-Barr Virus
Disease
Infectious mononucleosis; associated with Burkitt's lymphoma in East African children.

Characteristics
Enveloped virus with icosahedral nucleocapsid and linear double-stranded DNA. No virion polymerase. One serotype.

Transmission
Virus found in human oropharynx and B lymphocytes. It is transmitted primarily by saliva.

Pathogenesis
Infection begins in the pharyngeal epithelium, spreads to the cervical lymph nodes, then travels via the blood to the liver and spleen. EBV establishes latency in B lymphocytes.

Laboratory Diagnosis
The virus is rarely isolated. Lymphocytosis, including atypical lymphocytes, occurs. Heterophil antibody is typically positive (Monospot test). Heterophil antibody agglutinates sheep or horse red blood cells. A significant rise in EBV-specific antibody to viral capsid antigen is diagnostic.

Treatment
No effective drug is available.

Prevention
There is no drug or vaccine.
Herpesvirus 8
Causes Kaposi's sarcoma, especially in AIDS patients. Transmitted sexually. Diagnosis made by pathologic examination of lesion biopsy. See spindle cells and extravasated red blood cells. Purple color of lesions due to collections of red cells. No specific antiviral treatment and no vaccine.
+ Strand RNA
Picornavirus-polio, coxsackie, rhinovirus
Togavirus-Rubella, equine encephalitis
Retrovirus
Flavivirus
Coronavirus
Rubella
- Sense RNA
Influenza
Parainfluenza
RSV
Meales
Mumps
Rabies