Microbiology and Immunology

Lysogeny WORLD OF MICROBIOLOGY AND IMMUNOLOGY

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The treatment for Lyme disease is antibiotic therapy. If

a patient has strong indications of Lyme disease (symptoms

and medical history), the doctor will probably begin treatment

on the presumption of this disease. The American College of

Physicians recommends treatment for a patient with a rash

resembling EM or who has arthritis, a history of an EM-type

rash, and a previous tick bite.

The physician may have to adjust the treatment regimen

or change medications based on the patient’s response.

Treatment can be difficult because B. burgdorfericomes in sev-

eral strains (some may react to different antibiotics than others)

and may even have the ability to switch forms during the course

of infection. Also, B. burgdorferican shut itself up in cell niches,

allowing it to elude antibiotic actions. Finally, antibiotics can kill

B. burgdorferionly while it is active rather than dormant.

If aggressive antibiotic therapy is given early, and the

patient cooperates fully and sticks to the medication schedule,

recovery should be complete. Only a small percentage of

Lyme disease patients fail to respond or relapse (have recur-

ring episodes). Most long-term effects of the disease result

when diagnosis and treatment is delayed or missed. Co-infec-

tion with other infectious organisms spread by ticks in the

same areas as B. burgdorferi(babesiosis and ehrlichiosis, for

instance) may be responsible for treatment failures or more

severe symptoms. Lyme disease has been responsible for

deaths, but that is rare.

An genetically engineered vaccinefor Lyme disease

was made available in the United States in 1999. Immunity

requires three injections, the first two given a month apart; a

third injection given a year later. Clinical trials conducted in

1997 from a large study of 10,000 adults in many locations

showed strong promise of the vaccine’s safety and efficacy.

The Centers for Disease Controlrecommends the vaccine for

those who live and work in Lyme disease endemic areas, and

who have repeated and prolonged exposure to tick-infested

areas (e.g., park rangers, landscape workers). The Lyme dis-

ease vaccine will not prevent other diseases spread by ticks,

however, so protective measures against tick bites should still

be observed. The vaccine is not recommended for travelers

who will have little exposure when visiting areas where Lyme

disease has occurred.

Precautions to avoid contact with ticks include moving

leaves and brush away from living quarters. Most important

are personal protection techniques when outdoors, such as

using repellents containing DEET, wearing light-colored

clothing to maximize ability to see ticks, tucking pant legs into

socks or boot top, and checking children frequently for ticks.

LYMPHOCYTES•seeTCELLS ORTLYMPHOCYTES

LLysogenyYSOGENY

Lysogeny refers to a process whereby a virus that specifically

infects a bacterium, a bacteriophage(which means “devourer

of bacteria”), achieves the manufacture of copies of its

deoxyribonucleic acid(DNA) genetic material by integrating

the viral DNA into the DNA of the host bacteria. The inserted

viral DNA is then replicated along with the host DNA.

The nature of lysogeny remained unresolved for many

years following the discovery of the bacteriophage by Felix

d’Hérelle in 1915. The sudden appearance of virus in cultures

of bacteria was at first thought to be the result of viral con-

tamination. The acceptance of lysogeny as a real phenomenon

came almost 40 years later.

In lysogeny no new virus particles are made. Instead,

the virus essentially remains dormant, while ensuring that its

genetic material continues to be made. A stress to the bac-

terium, such as exposure of the bacterium to ultraviolet light,

triggers the viral DNA to separate from the bacterial DNA.

Then, new virus particles will form in what is known as the

lytic cycle. The two processes of lysogeny and lysis are under

a system of control first explained by the French biologist

André Lwoff in the early 1950s.

Lysogeny is of benefit to the virus, allowing the genetic

material to persist in the absence of a virus manufacture.

Lysogeny can also be beneficial to the host bacterium. The pri-

mary benefit to bacteria occurs when the integrated viral DNA

contains a genethat encodes a toxin. Possession of the toxin

can be advantageous to those bacteria that establish an infec-

tion as part of their strategy of replication. For example, tox-

ins encoded by bacteriophage genes are the main cause of the

symptoms associated with the bacteria diseases of tetanus,

diphtheria, and cholera.

The process of lysogeny has been studied most inten-

sively in a bacteriophage that is designated as lambda. In the

lambda bacteriophage, the establishment of lysogeny

depends on the presence of three viral proteins. These are

designated cI (“c-one”), cII, and cIII. The cI protein is man-

ufactured first, using host molecules that interpret the infor-

mation for the protein contained in the viral DNA, following

the entry of the viral DNA into the host bacterium. At this

point the viral DNA is not integrated into the host genome,

but exists as an independent circle. CI is a so-called repres-

sor protein that operates to occupy sequences on the viral

genome that would otherwise be used to make the various

viral proteins that are needed to assemble the new virus par-

ticles. By occupying these sites, cI prevents viral proteins

from being produced.

At about the same time, the viral DNA becomes inte-

grated into the host DNA and the cII and cIII proteins are man-

ufactured. These latter proteins assist cI in the task of blocking

synthesis of viral components. Accordingly, cI, cII, and cIII

function to maintain the lysogenic state. The cII protein func-

tions to make the manufacture of cI by the host’s transcription

machinery more efficient. The cIII protein helps protect the cII

protein from being degraded by host enzymes.

Once lysogeny is established, the continued manufac-

ture of the cI protein will maintain the integrated state of the

viral DNA.

The cI protein maintains its own transcription. The

binding of cI to a certain stretch of DNA promotes the recog-

nition and use of the gene for cI to manufacture the cI protein.

This is known as positive control. As well, the protein exerts a

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