SPECIFICAL INFLAMMATORY PROCESSES
OF THE MFA (ACTINOMYCOSIS, TUBERCULOSIS, SYFILIS), AIDS: CLASSIFICATION,
CLINICAL COURSE OF, DIAGNOSIS, TREATMENT. PMK
Cervicofacial Actinomycosis
Cervicofacial
actinomycosis is a disease that is characterized by the formation of abscess,
fistulae, tissue fibrosis and draining sinus tracts. This disease can mimic
many other conditions such as granulomatous disease and malignancy. They show
soft tissue swelling in the neck and head.Cervicofacial actinomycosis is caused
by bacteria known as Actinomyces israelii. This type of bacteria is usually
present in the mouth, however it is capable of causing disease once it enters
the tissues from an injured portion of the body. Actinomyces israelii anaerobic
meaning it dislikes oxygen and grows deep inside the tissues where oxygen level
is low. Root canal treatment, tooth extraction, poor dental hygiene or jaw
surgery are some of the reasons which allow access to Actinomyces israelii thus
causing an infection.
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ActinomycosisActinomycosis - the chronic illness caused by various kinds of Actinomyces. It is characterised by a lesion of various organs and tissues with formation of dense infiltrates which then abscess with the advent of fistulas and an original lesion of a skin. Actinomycosis aetiology
Originators - various kinds
of Actinomyces, or radiant mushrooms. The cores from them is the following:
Actinomyces israelu, Actinomyces bovis, Actinomyces albus, Ac. violaceus.
Actinomyces well grow on nutrient mediums, forming colonys of the irregular
form, is frequent with radiant edges. Are pathogenic for many kinds of
agricultural and laboratory animals. In a pathological stuff meet in the form
of druses which represent yellowish lumps in diameter of 1- Actinomycosis epidemiology
The actinomycosis is extended in all countries. With it humans and agricultural animals are ill. However cases of infestation of the human from sick humans or animals it is not described. Originators of an actinomycosis eurysynusic in the nature (hay, straw, bedrock, etc.). Actinomyces often find in healthy humans in an oral cavity, a debris, lacunas of tonsils, on a mucosa of a gastrointestinal tract. Matters both exogenous, and endogenous infestation means. Actinomycosis pathogenesis
The most frequent is the endogenous path of an infection contamination. Actinomyces eurysynusic in the nature, in particular on plants, can get with plants to an organism and be on mucosas as a saprophyte. Transition of Actinomyces from saprophytical in a parasitic state is promoted by inflammatory diseases of mucosas of an oral cavity, a respiratory and gastrointestinal tract. On a place of introduction of Actinomyces the infectious granuloma which sprouts in surrounding tissues is formed. In granulations there are abscesses which, breaking, form fistulas. The skin lesion has secondary character. In formation of pyeses the role and secondary, mainly staphylococcal infection contamination plays. Antigens of radiant mushrooms lead to a specific sensibilization and allergic rearrangement of an organism (a hypersensibilization of the slowed down phylum), and also to antibody formation (complement-linked, agglutinins, precipitin, etc.). Symptoms and actinomycosis flow
Duration of an incubation interval is not known. He can fluctuate over a wide range and reach till several years (from time of a becoming infected development of demonstrative forms of an actinomycosis). The basic clinical forms of an actinomycosis: 1. An
actinomycosis of a head, tongue and a neck 2. A thoracal actinomycosis 3. The abdominal 4. An actinomycosis of genitourinary
organs 5. A skin actinomycosis 6. A mycetoma 7. An
actinomycosis of the central excitatory system The actinomycosis concerns to initially-persistent infections with long progressing flow. At infiltrate growth the skin is involved in process. In the beginning very dense and almost painless infiltrate is defined, the skin becomes tsianotichno-crimson, there is a fluctuation, and then educe is long not healing fistulas. In pus find belovato-yellowish fine lumps (druses). Cervicofacial actinomycosis meets most often. On expression of process it is possible to secure the deep (muscular) form when process is localised in an intermuscular fat, hypodermic and dermal forms of an actinomycosis. At the muscular form process is localised mainly in masseters, under a fascia covering them, forming dense, cartilaginous consistences an infiltrate in the field of a mandible angle. The person becomes azygomorphous, the masticatory spasm of various intensity educes. Then in an infiltrate there are locuses of a ramollissement which are spontaneously dissected, forming the fistulas abjointing purulent or krovjanisto-purulent fluid, sometimes with an admixing of yellow grains (druses). A cyanotic coloration of a skin round fistulas it is long remains and is characteristic implication of an actinomycosis. On a neck original changes of a skin in the form of cross-section located platens are formed. At the dermal form of an actinomycosis infiltrates ball-shaped or semiball-shaped, localised in a hypodermic fat. A masticatory spasm and disturbances of processes of chewing it is not observed. The dermal form meets seldom. Actinomycotic process can grasp cheeks, labiums, tongue, tonsils, a trachea, orbits, a larynx. Flow rather congenial (in comparison with other forms). Thoracal actinomycosis (an actinomycosis of organs of a thoracal lumen and a thoracal side), or an actinomycosis of lungs. The beginning gradual. There is a delicacy, subfebrile temperature, tussis, in the beginning dry, then with a mucopurulent sputum, is frequent with a blood admixing (the sputum has an odour of the earth and taste of copper). Then the peribronchitis picture educes. The infiltrate extends from the centre to periphery, grasps a pleura, a thoracal side, a skin. There is a tumescence with extremely expressed stinging morbidity at a palpation, the skin becomes bagrovo-cyanotic. Fistulas educe, in pus druses of Actinomyces are found. Fistulas intercommunicate with bronchuses. They settle down not only on a thorax, but can appear on a loin and even on a hip. Flow serious. Without treatment patients die. On frequency the thoracal actinomycosis takes the second place. Abdominal actinomycosis also meets often enough (takes the third place). The primary locuses are more often localised in ileocecal range and in the field of an appendix (over 60 %), then there are other departments of a colon and the stomach or a thin intestine, an esophagus is very seldom amazed initially. The abdominal wall is amazed again. The primary infiltrate is localised in ileocecal range more often, quite often imitates surgical diseases (an appendicitis, impassability of an intestine, etc.). Extending, the infiltrate grasps also other organs: the liver, nephroses, a column, can reach an abdominal wall. In the latter case there are characteristic changes of a skin, the fistulas intercommunicating with an intestine. Are located usually in inguinal range. At an actinomycosis of a rectum infiltrates cause occurrence of specific paraproctites, fistulas are dissected in perianal range. Without etiotropic treatment the lethality reaches 50 %. Genital actinomycosis and Pelvic actinomycosis meets rare. As a rule, it is secondary lesions at infiltrate diffusion at an abdominal actinomycosis. Primary actinomycotic lesions of generative organs meet very seldom. Actinomycosis of bones and joints meets rare. This form arises or as a result of transition of an actinomycotic infiltrate from the next organs, or is a consequence of hematogenous drift of a mushroom. Osteomyelites of bones of an anticnemion, a basin, a column, and also a lesion patellar and other joints are described. Quite often process is preceded by a trauma. Osteomyelites proceed with a destruction of bones, formation of sequesters. Attracts attention, that despite the expressed osteal changes, sick keep ability to move, at lesions of joints function seriously is not broken. At formation of fistulas there are characteristic changes of a skin. Skin actinomycosis arises, as a rule, again at primary localisation in other organs. Skin changes become appreciable when actinomycotic infiltrates reach a hypodermic fat and are especially characteristic at formation of fistulas. Mycetoma - an original variant of an actinomycosis. This form was known for a long time, often enough met in the tropical countries. Disease begins with appearance on stop, mainly on a sole, one or several dense circumscribed knots in size from a pea and more, covered at first not variated skin, further over inspissations the skin becomes red-violet or brownish. In the neighbourhood with pristine knots appear new, the skin swells, autopodium is enlarged in volume, changes the form. Then knots are softened and dissected with formation of deeply going fistulas excreting purulent or is serous-purulent, sometimes bloody fluid, is frequent with a fetor. In abjointed fine grains of usually yellowish colour (druse) are appreciable. Knots are almost painless. Process slowly progresses, all sole is penetrated by knots, toes turn up. Then knots and fistulous courses appear and on autopodium back. All autopodium turns to the deformed and pigmented mass penetrated by fistulas and lumens. Process can pass to muscles, tendons and bones. The atrophy of muscles of an anticnemion is sometimes observed. Usually process grasps only one autopodium. Disease proceeds very longly (10-20 years). Complications. Stratification of a secondary bacteriemic infection contamination. The diagnosis and the differential diagnosis. In far come cases with formation of fistulas and characteristic changes of a skin the diagnosis of difficulties does not represent. It is more difficult to diagnose initial forms of an actinomycosis. For diagnostics the intracutaneous test with actinolysathos has some value. However in attention it is necessary to accept only positive and sharply positive assays as weakly positive intracutaneous tests often happen at patients to diseases of dens (for example at an alveolar pyorrhea). Assay Negative takes not always allow to exclude an actinomycosis as at patients with serious forms they can be negative owing to sharp oppression of cellular immunodefence, they are always negative at a HIV-infected. Abjection of culture of Actinomyces from a sputum, a mucosa of a fauces, a nose has no diagnostic value as Actinomyces are quite often found and in healthy faces. The reaction of binding complement with actinolysathos which happens positive at 80 % of patients has diagnostic value. The greatest diagnostic value has abjection (detection) of Actinomyces in pus from fistulas, in biopsy samples of the amazed tissues, in druses, in the last is sometimes microscopically mycelium strands are found only. In these cases it is possible to try to secure culture of Actinomyces by stuff sowing on medium of the Aloe. Actinomycosis of lungs is necessary for differentiating from neoplasms of lungs, abscesses, other deep mycoses (an aspergillosis, a nocardiosis, a histoplasmosis), and also from a pulmonary tuberculosis. The abdominal actinomycosis should be differentiated from various surgical diseases (an appendicitis, a peritonitis and so forth). A lesion of bones and joints-from of purulent diseases. Actinomycosis treatment
The best results are given by a combination of a causal treatment (antibiotics) and immunotherapies. At the is cervical-maxillofacial form prescribe inside a phenoxymethylpenicillin for 2 grammes/days and at duration of a course not less than 6 weeks. It is possible to prescribe also Tetracyclinum in the big doses (on 0,75 gramme 4 times a day within 4 weeks or on 3 gramme a day only in the first 10 days, and then on 0,5 gramme 4 times a day within last 18 days). Erythromycin is prescribed on 0,3 gramme by 4 times a day within 6 weeks. At abdominal forms and at an actinomycosis of lungs prescribe the big doses of a benzylpenicillin (10000000 Unit/day and more) intravenously within 1-1,5 months with the subsequent transition to a phenoxymethylpenicillin in a daily dose of 2-5 gramme within 2-5 months. At consecutive infection stratification (staphilococcuses, an anaerobic microflora) prescribe long courses of a dicloxacillin or antibiotics of tetracycline bunch, at a mephitic gangrene - metronidazole. For an immunotherapy actinolysathos it is possible to introduce subcutaneously or intradermally, and also it is intramuscular. Under a skin and intramusculary introduce on 3 ml actinolysathos 2 times a week. On a course of 20-30 injections, duration of a course 3 months At an abscess, an empyema spend surgical treatment (dissecting and a drainage). At extensive damages of a pulmonary tissue sometimes resort to a lobectomy. From antibiotics the most effective are Tetracyclinums, then go a phenoxymethylpenicillin and erythromycin is less effective. Refractory to these antibiotics of strains of Actinomyces did not meet. Actinomycosis forecast
Without etiotropic treatment the forecast serious. At an abdominal actinomycosis 50 % of patients died, at the thoracal all patients perished. Rather the is cervical-maxillofacial actinomycosis is easier proceeded. All it causes necessity of early diagnostics and the beginning of therapy before development of serious anatomical damages. Considering possibility of relapses, convalescents should be under long observation (6-12 months). Actinomycosis preventive maintenance
and actions in the locus
Hygiene of an oral cavity, timely treatment of dens, inflammatory changes of tonsils and an oral cavity mucosa. Specific preventive maintenance is not developed. Actions in the locus do not spend. |
Actinomycosis
Actinomycosis is a
long-term (chronic) bacterial infection that commonly affects the face and
neck.
Causes
Actinomycosis is
usually caused by an anaerobic bacteria called Actinomyces
israelii, which is a common and normally not disease-causing
(nonpathogenic) organism found in the nose and throat.
Because of the
bacteria's normal location in the nose and throat, actinomycosis most commonly
appears in the face and neck. However, the infection can sometimes occur in the
chest (pulmonary actinomycosis), abdomen, pelvis, or other areas of the body. The infection is not
contagious.
Symptoms occur
when the bacteria enters the facial tissues after trauma, surgery, or
infection. Common triggers include dental abscess or oral surgery. The infection has also been seen in certain women who
have had an intrauterine device (IUD) to prevent pregnancy.
Once in the
tissue, it forms an abscess, producing a hard, red to reddish-purple lump,
often on the jaw, from which comes the condition's common name, "lumpy
jaw."
Eventually, the
abscess breaks through the skin surface to produce a draining sinus tract.
Symptoms
A patient with Actinomycosis on the right side of the face.
Actinomycosis of Maxilla. The disease
spread to opposite side; finally implicated base of skull, and proved fatal. Treated by radium.
Exams and Tests
Treatment
Treatment of
actinomycosis usually requires antibiotics for several months to a year.
Surgical drainage or removal of the lesion may be needed. If the condition is
related to an IUD, the device must be removed.
Outlook
(Prognosis)
With treatment,
you should recover fully.
Possible
Complications
Meningitis can rarely develop from this infection.
When to Contact a
Medical Professional
Call your health
care provider if you develop any of the symptoms of this disorder. Beginning
treatment promptly helps quicken the recovery.
Prevention
Good oral hygiene and regular dentist visits may help prevent some forms of actinomycosis.
Alternative Names
Lumpy jaw
Actinomycosis is an infection caused by a bacterium called Actinomyces
israelii (A. israelii).
Actinomycosis (also known as Rivalta disease, big jaw, clams, lumpy jaw
or wooden tongue) is an infection, commonly of the face and neck, that produces
abscesses (collections of pus) and open-draining sinuses (tracts in the skin).
Actinomycosis is caused by a bacterium called Actinomyces israelii (A.
israelii). It occurs normally in the mouth and tonsils. This bacterium may
cause infection when it is introduced into the soft tissues by trauma, surgery or another infection. Once in the tissues, it may form an
abscess that develops into a hard red to reddish purple lump. When the abscess
breaks through the skin, it forms pus-discharging lesions.
Actinomycosis is caused by a strain of bacteria called actinomycetales.
Actinomycetales are found in many of the body’s cavities, such as inside the
mouth and less commonly the bowel.
In women, they can also be found in the womb and the fallopian tubes
(through which eggs are released into the womb).
How actinomycosis spreads
Actinomycetales are anaerobic bacteria, which means they cannot survive
in oxygen-rich environments. Therefore, they do not present a problem when they
are in one of the body’s cavities, such as the mouth or the intestinal
tract.
However, if actinomycetales break through the protective lining (mucus
membrane) that surrounds the cavities, they can penetrate deep into your body’s
tissue. As the deep layers of human tissue are low in oxygen, the bacteria are
able to reproduce quickly and infect healthy tissue.
In an attempt to combat the infection, your immune system (the body’s natural defence
against infection and illness) will send infection-fighting cells to the source
of the infection. However, these cells do not have the ability to kill the
bacteria and will quickly die.
As the infection-fighting cells die, they accumulate into a
yellowish-coloured liquid called pus. Having failed to kill the infection, your
immune system will attempt to limit its spread by using healthy tissue to form
a protective barrier around the pus. This is how a pus-filled swelling, known
as an abscess, is formed.
Unfortunately, the actinomycetales strain of bacteria has the ability to
penetrate the protective barrier of an abscess and move into more healthy
tissue. Your immune system will attempt to counter the infection by producing
more abscesses.
Your body will eventually need to get rid of the accumulation of pus. To
do this, small channels called sinus tracts will develop that lead from the
abscesses to the surface of your skin.
The sinus tracts will leak pus, as well as ‘sulphur granules’, which are
a yellow, powdery substance. The sulphur granules are actually made up of lumps
of bacteria, but they are known as sulphur granules as they are the same colour
as the chemical sulphur.
Opportunistic infection
Actinomycosis is an opportunistic infection that does not cause any
symptoms unless an opportunity arises for it to penetrate into the body‘s
tissue.
Opportunities for oral cervicofacial actinomycosis include:
Most cases of thoracic actinomycosis are thought to be caused by small
particles of food or other ingested material that get mixed up with the
actinomycosis bacteria. Rather than passing harmlessly down into the stomach,
the particles are mistakenly passed down into the windpipe and the airways of
the lungs.
People with long-term drug or alcohol problems are particularly at risk
of developing thoracic actinomycosis for two reasons:
Abdominal actinomycosis occurs when something tears the wall of the
intestine (bowel), allowing the bacteria to penetrate into deep tissue.
The intestine can tear as a result of an infection, such as a burst
appendix that damages the wall of the intestine. Or it can be damaged
through injury – for example, when someone mistakenly swallows a fish bone.
There have also been some reported cases of abdominal actinomycosis
occurring as a complication of bowel or abdominal surgery.
Most cases of pelvic actinomycosis have been recorded in women who were
using the intrauterine device (IUD) form of contraception. The IUD is a
small, T-shaped contraceptive device made from plastic and copper that fits
inside the womb. The women affected tend to be long-term users of the IUD
(eight years or more).
One explanation for the high number of cases of pelvic actinomycosis in
women who are using the IUD is that over time the IUD may damage the womb lining,
allowing bacteria to penetrate into deep tissue. However, no research has yet
been done to find out whether or not this is the case.
It should be stressed that developing pelvic actinomycosis as a result of using an
IUD is very unlikely. In
The list of signs and symptoms mentioned in various sources for
Actinomycosis includes the 17 symptoms listed below:
Medical Care
In most cases of actinomycosis, antimicrobial therapy is the only
treatment required, although surgery can be adjunctive in selected cases. Penicillin G is the drug of choice for treating
infections caused by actinomycetes.
Surgical Care
Attempt to cure actinomycosis, including extensive disease, with
aggressive antimicrobial therapy alone initially. Surgical therapy may include
incision and drainage of abscesses, excision of sinus tracts and recalcitrant
fibrotic lesions, decompression of closed-space infections, and interventions
aimed at relieving obstruction (eg, when actinomycotic lesions compress the
ureter).
Consultations
Diet
No specific dietary precautions are indicated in patients with
actinomycosis.
Activity
Patients with actinomycosis may be active to the degree tolerated.
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Figure
1 |
Figure
2 |
A 58-year-old
previously healthy man presented to the emergency center with a 12-month
history of progressive right-sided facial swelling. The patient reported only
mild pain exacerbated by eating and difficulty opening his mouth. He denied
fever, chills, or weight loss. He had a 40-pack per year history of smoking
tobacco and consumed 40 ounces of beer per day. The patient had no
significant past medical history, and denied diabetes, hypertension, or cancer.
He had lived his entire life in
ORAL MANIFESTATIONS OF TB DISEASE
The estimated prevalence of oral tuberculous lesions ranges from 0.05 to
5%. Oral lesions are usually secondary, reflecting oral inoculation
with infected sputum or as a result of hematogenous spread. Rare
cases of primary tuberculous involvement of oral structures have been
reported. In one study evaluating patients with TB disease and
co-infection with HIV, the prevalence of oral tuberculous lesions was found to
be 1.33%. Oral tuberculous lesions are nonspecific in their clinical
presentation, and their consideration in the differential diagnosis requires a
high degree of awareness. While all oral tissues may be affected, in the cohort
of patients with both TB disease and HIV-infection, the palate and dorsum of
the tongue (Figure 2) were the most frequent sites of oral involvement.
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Figure 2. |
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Oral
tuberculous lesion of the dorsum of the tongue in a patient with both TB
disease and HIV infection. |
These data are in agreement with those reported by other investigators
in patients with TB disease without HIV-infection. Pain and cervical
lymphadenopathy are common but not universal findings. A rare case of
tuberculous osteomyelitis of the mandible and several cases of tuberculous
parotitis have been documented.
Diagnosis
Early diagnosis of infection with MBT is important because of the nature
of the disease. The tuberculin skin test (TST) or a blood assay for
Mycobacterium tuberculosis (BAMT) are useful for screening groups of people for
LTBI with exposure rates that substantially exceed those of the general
population (Table 1).
The TST, which is the Mantoux intradermal test, using 5 tuberculin units
of Tween-stabilized purified protein derivative (PPD)-tuberculin is the
traditional method of diagnosing LTBI. The antigen is injected
intracutaneously into either the volar or dorsal surface of the forearm.
In patients with LTBI, the TST evokes a delayed hypersensitivity reaction to
the tuberculin mediated by T-lymphocytes producing an area of redness and
swelling. The test is read at 48 to 72 hours. Erythema is
disregarded, and the diameter of the induration is measured (Table 3).
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Table 3.
Interpreting the tuberculin skin test reaction.1 |
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Induration
of 5 mm |
Induration
of 10
mm |
Induration
of 15
mm |
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People with HIV infection |
Foreign-born persons |
People with
no risk factors for TB |
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Close
contacts of people with TB |
HIV-negative
persons who use illicit drugs People with no risk factors for TB |
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People who
have had TB disease before |
People in residential facilities |
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Illicit drug users |
Children £4 years of age |
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While the relative
specificity of the TST skin test is high, both false positive and false
negative reactions have been reported. False-positive reactions may be due to
previous sensitization with mycobacterial antigens, as may be seen following
vaccination with Bacille Calmette-Guerin (BCG). False-negative reactions to the
TST have been reported in immunocompromised patients, in patients with recent
exposure to MBT, and in very young children.
The CDC recommends
persons with a positive TST undergo further evaluation.46 In recent years a number of in vitro diagnostic tests in the form of
BAMT have been developed. However, the QuantiFERON®-TB Gold (QFT-G) test is the
only such test approved by the Food and Drug Administration (FDA) for the
detection of latent TB infection. This test detects the release of
interferon-gamma in fresh heparinized blood from sensitized persons when it is
incubated with mixtures of synthetic peptides representing two proteins present
in MBT. The sensitivity of QFT-G is statistically similar to that of TST for
detecting TB infection. However, the QFT-G measures cell-mediated response to
peptides from two MBT proteins that are not present in any BCG vaccine strains
and are absent from the majority of mycobacteria other than MBT. Hence, the
QFT-G has greater selectivity.
Although the history, physical examination, TST and/or QFT-G data, and
other studies such as chest radiographs are helpful and at times may strongly
suggest TB disease, definitive diagnosis usually requires the demonstration of
MBT in the patient's tissues or secretions.1 Bacteriologic examination, which includes obtaining a specimen of
sputum, detection of acid-fast bacilli (AFB) in stained (Ziehl-Neelsen method)
smears examined microscopically, may provide the first bacteriologic clue to TB
disease. However, not all AFB are tubercle bacilli, therefore, a positive
bacteriologic culture for MBT is essential to confirm the diagnosis. DNA probes
specific for the genus Mycobacterium now are used routinely to identify
specific mycobacterium. When the presence of MBT has been confirmed, it is then
necessary to perform drug susceptibility testing on positive cultures.
Immunization with viable Mycobacterium bovis BCG is the most widely used
preventive measure to control tuberculosis worldwide. Administered to newborns
in a single dose, it prevents severe disease and reduces mortality among
children from miliary and meningeal disease. However, BCG does not protect
against pulmonary tuberculosis in children or adults. As mentioned earlier,
optimal immune response to MBT infection appears to involve both CD4+ and CD8+
T-cells. BCG activates CD4+ T-cells by being taken up by macrophages and
residing within phagosomes which are membrane-enclosed vacuoles. These
antigens, once processed in the phagosomes, then readily interact with MHC
class II molecules. However, the ability of the bacillus to block acidification
of the phagosomes precludes its release into the cytoplasm and for an antigen
to bind to MHC class I molecules it must be processed in the cytoplasm of the
infected cells. Consequently, BCG fails to elicit a CD8+ T-cell response. A
recently developed recombinant bacillus with an impaired ability to counter the
acidification of phagosomes will soon enter phase 1 clinical trials. This new
vaccine is likely to be more effective because it targets both CD4+ and CD8+
T-cells.
The goal of antibacterial chemotherapy is to induce selective toxicity. Selectivity can be realized by attacking
targets that are:
One target is the bacterial cell wall, a structure that is both unique
and essential for the survival of most pathogenic bacteria. The bacterial cell
wall is a three-dimensional meshwork of peptide-crosslinked sugar polymer
(peptidoglycan or murein) surrounding the cell just outside its cytoplasmic
membrane.
Bacteria may be conveniently divided into two groups, Gram-positive and
Gram-negative, based on the relative abilities of bacteria to retain purple
Gram-stain after being washed with an organic solvent such as acetone.
Gram-positive bacteria retain the stain and appear purple, whereas
Gram-negative bacteria lose the stain and appear pink. The ability to retain stain
results from two distinguishing characteristics of cell wall architecture. In
Gram-positive bacteria, the cell wall is composed of a thick layer of murein
(Figure 3A). The murein layer in Gram-negative bacteria is thinner but it is
surrounded by a second, outer lipid bilayer membrane (Figure 3B). The cell wall
of mycobacteria, which include the causative agent of tuberculosis, is similar
to that of Gram-negative bacteria (Figure 3C).
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Figures
3A-C, Gram-positive and Gram-negative bacteria |
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Figure 3A. |
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In
Gram-positive bacteria, the cell wall is composed of a thick layer of murein. |
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Figure 3B. |
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The murein
layer in Gram-negative bacteria is thinner but it is surrounded by a second,
outer lipid bilayer membrane. |
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Figure 3C. |
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The cell
wall of mycobacteria, which includes the causative agent of tuberculosis, is
similar to that of Gram-negative bacteria. The main difference being
mycobacteria has a thick outer membrane composed of two leaflets that are
asymmetrical in size and composition. |
Both Gram-negative bacteria and mycobacteria are enclosed by an inner
cytoplasmic membrane, a thin murein layer, and an outer membrane. The main
difference is that, in mycobacteria, the outer membrane is thick, composed of
two leaflets that are asymmetrical in size and composition. The inner leaflet
is composed of arabinogalactan and mycolic acid, and the outer leaflet is
composed of extractable phospholipids. Cell wall biosynthesis takes place in
the following three major steps:
1. Synthesis of murein monomers from amino acids and sugar building blocks
(N-acetylglucosamine [NAG] and N-acetylmuramic acid [
2. Polymerization of the monomers into linear peptidoglycans.
3. Crosslinking of the polymers into a three-dimensional meshwork.
In mycobacteria the
Standard antimycobacterial treatment regimens include antibiotics that
target unique targets such as the synthesis of NAG-arabinogalactan and the
early steps in mycolic acid synthesis (Table 4).
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Table
4. Antimycobacterial agents. |
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First-line Drugs: |
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Drug |
Mechanism
of Action |
Adverse
Drug Effects |
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Ethambutol |
Inhibits arabinosyl tranferase |
Optic
neuritis |
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Pyrazinamide |
Inhibits fatty acid synthetase |
Morbilliform rash |
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Isoniazid |
Inhibits fatty acid synthetase |
Hepatitis |
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Rifamycins: |
Bind to RNA
polymerase and inhibit transcription |
Hepatitis |
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Second-line Drugs: |
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Cycloserine |
Inhibits monomer synthesis |
Psychosis |
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Ethionamine |
Inhibits fatty acid synthetase |
Hepatitis |
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Aminoglycosides: |
Bind to the
30S ribosomal subunit and inhibit translation |
Ototoxicity |
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Fluoroquinolones: |
Inhibit
topoisomerase II (DNA gyrase), thereby releasing DNA with staggered
double-stranded breaks |
Nausea |
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Aminosalicylic acid |
Competitive
para-aminobenzoic acid antagonist |
GI disturbances |
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Combination Drugs: |
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Rifamate |
isoniazid + rifampin |
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Rifater |
isoniazid + rifampin + pyrazinamide |
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The treatment of infections with MBT can be divided into treatment of
LTBI and treatment of TB disease. Guidelines with detailed management
recommendations are published and updated regularly.
The risk for progression from LTBI to TB disease is highest during the
first two years after infection and is often predicated on concomitant medical
conditions that alter the ability of the immune system to maintain the
isolation of MBT (Table 2). HIV infection is the most important risk
factor. It has been estimated persons infected with MBT and
co-infected with HIV have a 6-10% risk per year of developing TB disease, while
an immunocompetent person infected with MBT has a 10% life-time risk for TB
disease. Isoniazid, given for nine months in a single daily dose, is
the drug of choice for the treatment of LTBI. Persons exposed to
patients with known isoniazid resistant TB disease and those with intolerance
to isoniazid may be treated with rifampin for four months. For
patients with known exposure to multi-drug resistant TB disease, a regimen with
two drugs to which MBT is susceptible is recommended for nine to 12 months.
Active
tuberculosis (TB) is very contagious. The World Health Organization (WHO)
estimates that one-third of the world's population is infected with the bacteria that cause TB.
To avoid getting an
active TB infection:
A TB vaccine (bacille
Calmette-Guerin, or BCG) is used in many
countries to prevent TB. But this vaccination is almost never used in the
Oral manifestations of syphilis
The past decade has shown a significant rise in the prevalence of
infective syphilis in the developed world, and striking increases in its
frequency have occurred in Eastern Europe, particularly the
CHANGING EPIDEMIOLOGY OF INFECTIVE
SYPHILIS
Infective syphilis is caused by the anaerobic filamentous spirochete, Treponema pallidum. In the past
decade there has been a significant rise in the prevalence of infective
syphilis in the developed world. Striking increases in the frequency of
syphilis have occurred in Eastern Europe, and smaller rises have been reported
in Western Europe and the
PRIMARY SYPHILIS
The mouth, perhaps surprisingly, is rarely the site of primary syphilis,
and because of its transient nature, the oral ulceration of primary syphilis
often goes unnoticed by the patient or by any unsuspicious clinician. In addition,
albeit rarely, the lesions of primary disease may be confused with other
pre-existing mucocutaneous disease. A chancre develops within 1 to 3 weeks of
acquisition. Primary syphilis is usually the consequence of orogenital or
oroanal contact with an infectious lesion. Kissing may, very rarely, cause
transmission; indeed, it has been suggested that intrafamilial oral acquisition
of syphilis in a child may have occurred via this route, although more usually
oral syphilis in a child is indicative of sexual abuse.
Primary syphilis of the mouth manifests as a solitary ulcer usually of
the lip or, more rarely, the tongue. The upper lip is more commonly affected
than the lower in males, while the opposite occurs in females—probably
reflecting the anatomy involved with fellatio and cunninlingus. The pharynx or
tonsils may rarely be affected. The ulceration is usually deep, with a red,
purple, or brown base and an irregular raised border. There is usually an
accompanying cervical lymphadenopathy. The ulceration of primary syphilis may
be confused with other solitary ulcerative disorders, most notably traumatic
ulceration, squamous cell carcinoma, and non-Hodgkin's lymphoma.
The diagnosis of primary syphilis may be aided by detailed analysis of
the sexual and/or social lifestyles of the patient and of any of the available
sexual partner; however, often the diagnosis of early disease can be difficult.
Affected patients often do not have a positive nonspecific reaginic test, eg,
Rapid Plasma Reagin (RPR) or Venereal Disease Reference Laboratory (VDRL)
tests. The specific tests for IgG antibodies to T. pallidum become positive before the reaginic
tests, and thus should be carried out when the nonspecific tests prove negative
but a diagnosis of primary disease is still likely.
Treponemes are present in primary lesions and can be detected by dark
field microscopy; however, this test is fraught with the risk of nosocomial
transmission and is thus no longer considered suitable. In addition, there can
be confusion between the spirochetes ofT. pallidum with the normal commensals of the
mouth.
Histopathology is not always helpful, as there are no specific
histopathological features, and the detection of T. pallidum with Warthin-Starry stain or silver
nitrate stain may not be possible. Monoclonal anthodyl immunoperoxidase
staining techniques can detect T.
pallidum and is a relatively
routine clinical investigation of biopsy material. However, molecular methods
such as in situ and tissue PCR still remain nonroutine investigations for all
types of syphilis. The tests used to detect IgM antibodies to T. pallidum may detect early infection.
OUTCOMES OF THERAPY
The primary chancres spontaneously heal within 7 to 10 days, although
they can persist much longer, only resolving with appropriate antimicrobial
therapy.
SECONDARY SYPHILIS
The features of secondary syphilis reflect the hematogenous spread of T. pallidum, and similarly to
its other mucocutaneous features, the oral manifestations of secondary syphilis
can be more extensive and/or variable than those of the primary disease. Oral
lesions arise in at least 30% of patients with secondary syphilis, although
very rarely oral ulceration may be the only manifestation of infection. The 2
principal oral features of secondary syphilis are mucous patches and
maculopapular lesions, although nodular lesions may rarely arise.
MACULOPAPULAR
LESIONS
ULCERONODULAR DISEASE (LUES MALIGNA)
Ulceronodular disease is an explosive generalized form of secondary
syphilis characterized by fever, headache, and myalgia, followed by a
papulopustular eruption that rapidly transforms into necrotic, sharply
demarcated ulcers with hemorrhagic brown crusts, organized in rupioid layers
commonly on the face and scalp. The mucosa is involved in about one third of
affected patients. Lues maligna gives rise to crateriform or shallow ulcers on
the gingivae, palate or buccal mucosa, with multiple erosions on the hard and
soft palates, tongue and lower lip.
NODULAR DISEASE
Rarely, secondary syphilis can manifest as nodules alone. This nodular
eruption of syphilis has a predilection for the face, mucous membranes, palms
of the hands and soles of the feet.26 Lesions may occur on the vermillion,
mimicking squamous cell carcinoma or keratoacanthoma.
DETECTION OF INFECTION IN SECONDARY DISEASE
Treponema pallidum can usually be detected on the
surface of erosions or ulcers by darkfield microscopy, although as noted above,
this test should be avoided. The patient will have positive serological tests.
The histopathological features of secondary syphilis are variable. Often
the changes are nonspecific, although they may include perivascular infiltrates
with a preponderance of plasma cells and epidermal psoriasiform hyperplasia.
Warthin-Starry strains will only detect spirochetes in about a third of
instances, although newer methods may increase the in situ detection of the
causative agent.
OUTCOMES OF THERAPY
The lesions of secondary syphilis will resolve spontaneously within 3 to
12 weeks, regardless of therapy, and about 25% of untreated patients will have
recurrence of secondary disease.
LATENT SYPHILIS
In early latent syphilis, usually the first 12 months after secondary
disease, affected patients are infectious. In late latent syphilis the
infectivity falls.
TERTIARY SYPHILIS
Clinical disease arises in about one third of patients with untreated
secondary syphilis. The oral complications of tertiary syphilis center upon
gumma formation, and much more rarely, syphilitic leukoplakia (and risk of oral
squamous cell carcinoma) and neurosyphilis.
GUMMA FORMATION
Gummas tend to arise on the hard palate and tongue, although very rarely
they may occur on the soft palate, lower alveolus, and parotid gland.27-30 A gumma
manifests initially as 1 or more painless swelling.16 When multiple, they tend to coalesce,
giving rise to serpigninous lesions. The swellings eventually develop into
areas of ulceration, with areas of breakdown and healing. There may be eventual
bone destruction, palatal perforation, and oro-nasal fistula formation. Rarely,
a gumma may erode into blood vessels—eg, the inferior alveolar artery. Gumma
manifests radiologically as ill-defined radiolucencies that may resemble
malignancy. The areas of ulceration eventually heal, although the resultant
scarring can, at least on the tongue, cause fissuring.
SYPHILITIC LEUKOPLAKIA AND RISK OF SQUAMOUS CELL CARCINOMA
Syphilitic leukoplakia would appear to be a homogenous white patch
affecting large areas of the dorsum of the tongue. There are few good
descriptions of syphilitic leukoplakia, and it is unclear whether this lesion
truly reflects syphilis, or more likely a tobacco smoking habit—indeed this was
observed by
An association between tertiary syphilis and oral squamous cell
carcinoma—particularly of the tongue—has been suggested for many years. Both
clinically- and serologically-based studies have suggested an increased
prevalence of syphilis in patient groups with squamous cell carcinoma of the
tongue (up to 60% in one study), the association being stronger in males than
females.31 A
relatively recent study of 16,420 people with syphilis resident in the US found
a significantly raised frequency of cancer of the tongue (and Kaposi's sarcoma)
in males.32 A
noncontrolled study found that 5 of 63 UK patients with squamous cell carcinoma
of the tongue had serological evidence of past syphilis as detected by both
specific and nonspecific tests.33 However,
it remains unclear whether any risk of oral squamous cell carcinoma in syphilis
is a direct consequence of infection (which seems unlikely) or is the effect of
recognized causative factors for oral malignancy, ie, tobacco, alcohol, and
malnourishment.
NEUROSYPHILIS
Aside from the well-recognized Argyll Robertson pupil, tertiary syphilis
can give rise to both unilateral and bilateral trigeminal neuropathy and facial
nerve palsy. Potentially, syphilitic osteomyelitis may give rise to trigeminal
neuropathy.
DETECTION OF INFECTION IN TERTIARY DISEASE
Gummas are characterized histopathologically by endarteritis obliterans,
necrosis with epithelioid and giant cells and a plasma cell infiltrate.
Spirochetes are difficult to detect. In tertiary disease, the nonspecific tests
may not be positive; the most reliable test is FTA, although this may remain
positive even after successful therapy.
CONGENITAL SYPHILIS
As discussed previously, in some communities there is a rising
prevalence of congenital syphilis. Treponema
pallidum crosses the placenta
only after the 16th week of intrauterine life; hence, depending upon the time
of infection, it may variably affect the facial structures. Resembling its
systemic features, the orofacial manifestations of congenital syphilis can be
split into early and late. Early features include diffuse maculopapular rash,
periostitis (frontal bossing of Parrot), and rhinitis. Late features,
manifesting at least 24 months after birth, comprise the Hutchinsonian triad of
interstitial keratitis of the cornea, sensorineural hearing loss, and dental
anomalies.
The dental anomalies of congenital syphilis only arise in teeth in which
calcification occurs during the first year of life, hence typically the
permanent incisors and first molars. Of note, the maxillary incisors are more
commonly affected than the mandibular ones. The incisors have a screwdriver
shape, there being a convergence of the lateral margins towards the incisal
edge. In some, there may be notching of the incisal edge, while in others,
there may be a depression on the labial surface. The first molar may be
bud-shaped and reduced to the size of the adjacent second molar. The normal
mesiodistal convexity of the crown may be reduced. Enamel hypoplasia may occur.
Yellow discoloration of the skin about the lips can arise soon after birth; the
area then becomes increasingly rigid with crack formation and eventual
(Parrot's) radial scars—rhagades—of the lips. There may be a loss of the
well-circumscribed border of the vermillion.
Other, less common orofacial features include atrophic glossitis and a
high, narrow palatal vault. Facial neuropathies may rarely occur as can palatal
gumma in adulthood.
INTERACTIONS BETWEEN HIV AND SYPHILIS
According to WHO,
Strong evidence supports several biologic mechanisms through which
sexually transmitted diseases (STDs) facilitate HIV transmission by increasing
both HIV infectiousness and HIV susceptibility. Thus, the detection of STDs and
the establishment of effective treatment is an important strategy of HIV
control.
INFLUENCE OF HIV DISEASE UPON SYPHILIS
It was initially suggested that concurrent HIV infection and syphilis is
not uncommon, particularly in young adults, men having sex with men, and
traders of commercial sex. HIV disease might significantly influence the
clinical source of syphilis, as it does for some STDs and other conditions
related to HIV-associated immune deficiency, and the associated infection is
often more aggressive than the mono-infection. A Nigerian study of 31 people
with concurrent HIV infection and syphilis found that 64.2% of the patients had
developed unusual lesions affecting more than 50% of the body. Also, the
chancres seen at the sites of inoculation had an atypical appearance.
However, a recent detailed study suggests that other than an increased
number and frequency of genital ulcers in secondary disease, HIV disease does
not greatly impact the clinical care of syphilis. Nevertheless, there have been
reports of prolonged primary disease and secondary disease; additionally,
neurosyphilis may present more quickly and ulceronodular disease is more likely
in patients infected with HIV than in those not infected.
INFLUENCE OF ORAL SYPHILIS UPON HIV DISEASE
Patients with concurrent HIV infection and syphilis usually have a
history of sexually transmitted infection, and it is common that these patients
have more than 1 condition (eg, genital ulcers, injected drug addition, etc)
that are potential sources of exposure. The genital ulceration of syphilis
increases the risk of HIV transmission. Nonulcerative STD, however, also have
the capacity of increasing the likelihood of HIV transmission, and the
detection and treatment of syphilis can probably help to reduce HIV
transmission. While there are no data to support the notion, it is likely that
oral syphilis principally influences HIV disease by increasing the likelihood
of HIV transmission (and other related viruses) by oral sexual routes. A recent
study found no association between early syphilis and changes in blood or semen
viral load or CD4 count in HIV-positive individuals. According to the study,
increased HIV-1 infectivity associated with early syphilis is unlikely to be
associated with increased levels of HIV-1 RNA in blood or semen. There is now
compelling evidence, based upon case and epidemiological studies, that HIV can
be transmitted via orogenital contact. In addition, as persons in high-risk
groups for HIV move away from high-risk sexual activities, there is likely to
be an increased frequency of orogenital contact, and hence oral sex will
contribute to a greater frequency of new infections than previously. Oral
ulcerative disease, such as that of all the stages of syphilis, will increase
the HIV load in the mouth, and hence the potential for HIV transmission via
oral sex.44 In
addition, this increased risk of HIV transmission will be further worsened by
ulcerative disease secondary to the use of the recreational drugs, crack
cocaine45 and cocaine
powder. Finally the oral ulcerative disease of syphilis is likely to increase
the nonsexual spread of human herpes virus 8 (HHV-8).
HOW DOES HIV AFFECT THE MOUTH?
In the early years of the HIV epidemic, dentists were often the first
health professionals to notice signs of a weak immune system. These signs were
infections that are normally controlled by a healthy person. When people get
tested for HIV infection and get treatment, most of these infections never show
up. However, many people do not get tested for HIV. They may be infected and
now know it. Regular dental care is an important way they may learn they have a
weak immune system.
According to the US Health Resources and Services Administration, over
one third of people with HIV will have at least one major oral health problem,
and almost two thirds do not receive regular dental care.
Pain or bleeding in your mouth can be a sign of infection. It can keep
you from eating normally. Severe pain makes some people skip taking their
medications. Serious infections in your mouth can cause other health problems.
Be sure to see a dentist or let your health care provider know if you have
trouble swallowing, changes in how food tastes, or pain or other problems with
your mouth or teeth.
Some dentists or their office staffers do not want to treat patients
with HIV. This goes against
community standards and violates the Americans with Disabilities Act. Dental health care workers
know how to protect themselves from diseases carried in the blood of their
patients, including HIV.
WHAT ARE THE SIGNS OF HIV IN THE MOUTH?
Several problems with the teeth, mouth and gums can show up in people
with HIV. These are discussed
below.
Dry Mouth and Tooth Decay
Many people with HIV have dry mouth. They don’t make enough saliva to chew and
swallow comfortably. Saliva protects teeth and gums from infection and decay.
HIV infection can cause dry mouth. So can some medications, as well as
coffee, carbonated beverages, alcohol, and smoking. If you have dry mouth, take
frequent drinks of water. You can talk to your health care provider about using
sugar-free gum or candy, or a saliva substitute.
Candidiasis (thrush) This infection is caused by a fungus
(yeast) called Candida. It shows up as red patches on the tongue or roof of the
mouth or white lumps that look like cottage cheese that can form anywhere in
the mouth. Candidiasis infection can move into the throat. It can also cause
painful cracks at the corners of the mouth called angular chelitis. Many
anti-fungal treatments can treat thrush. However, some cases of thrush are
resistant to the usual medications.
Canker sores (apthous ulcers) are small, round sores on the inside the cheek, under the tongue, or in
the back of the throat. They usually have a red edge and a gray center. The
sores can be quite painful. They can be caused by stress or by certain foods
such as eating too many tomatoes. Hot and spicy or acidic foods or juices make
them hurt more. Some ointments, creams or rinses can help.
Cold sores are caused by herpes simplex a common infection. In people with HIV,
cold sores can be more severe and can keep coming back. The most common
treatment is the antiviral drug acyclovir.
Gum Disease (periodontitis or gingivitis) is swelling of the gums. Sometimes painful
and bloody, it can progress from gum loss to loosening and even loss of teeth.
This can happen as quickly as 18 months. Dry mouth and smoking can make gum
disease worse. Brush your teeth, floss, and see a dentist regularly.
Recently, gum disease has been linked to higher levels of inflammation,
throughout the body. This can increase the risk of heart disease and stroke.
Hairy Leukoplakia is an irritation that usually shows up as painless, fuzzy white patches
on the side of the tongue. It can be an early sign of HIV infection.
Kaposi’s Sarcoma (KS), usually shows up
as dark purple or red spots on the gums, the roof of the mouth, and the back of
the tongue. It is rarely seen when people are tested early and start using
antiretroviral therapy for HIV infection. It can be the first sign of HIV
infection in people who have not been tested for HIV. The best treatment for
oral KS in someone with HIV is effective antiretroviral therapy.
Oral Warts - Human Papillomavirus, HPV is a sexually transmitted disease. Some strains of HPV cause warts or
cancer. HPV warts can show up in the mouth. The warts can be frozen or cut out.
Signs of HIV infection often show up in the mouth. You might know people
who haven’t been tested for HIV. Encourage them to pay attention to any mouth
problems.
Keep your mouth healthy by brushing your teeth and flossing. Get your
teeth cleaned regularly by a dental health professional. See a health or dental
care provider about any serious issues.
The following may
be warning signs of infection with HIV:
Thrush is a common problem for infants since their immune systems are not yet
fully developed. In healthy adults, however, thrush infections happen only
rarely, and usually are an indication of a lowered immune response.
Often it is due to illnesses other than AIDS such as general viral infections
or stress related fatigue. It is characterized by creamy white, soft
plaques that are easily
scraped off the
mucosa (the lining of the mouth) revealing a red, inflamed patch
underneath. This type is seen in the picture to the right. It is
easily treated with topical antibiotics like Nystatin.
The image above,
top left shows pharyngeal
candidiasis. The pharynx is the throat, and pharyngeal
candidiasis is an indication of the severe immune system depression
characteristic of AIDS. This form of yeast infection was considered pathognomonic of AIDS until
it was realized that persons who use inhaled
steroid medications for
the treatment of asthma are also prone to this sort of infection. (Once
again, the presence of pathognomonic signs of a disease, --which means
observable things that are frequently associated with a particular disease-- do
not necessarily mean that the patient has that disease, but a blood test is
strongly recommended in such cases.) Oral and pharyngeal
candidiasis are not contagious.
Angular cheilitis
is a very common condition. It is a fungal infection of the corners of
the lips. It can plague healthy people who tend to have moist lips,
especially in the cold winter months. This condition is caused by a
persistent fungal infection, and left untreated, tends to remain active for
many months. It generally looks like a reddened, dry area at the
corners of the l
ips. The
severe, white, ulcerated variety shown to the left is more indicative of the
type seen in AIDS. Even a severe case like this, by itself, does not
indicate that the patient has AIDS. It is easily treated with Nystatin
cream which is simply an antibiotic that kills the fungus. Angular
cheilitis is not contagious. click the image on the left to see more
images of angular cheilitis.
Hairy leukoplakia
is one of the most common HIV associated oral signs. It is a white,
corrugated or "hairy" "coating" on the lateral borders of
the tongue. Unlike thrush, it is not easily scraped off. It is
painless, but patients occasionally complain of its appearance and
texture. It is caused by the body's reaction to the Epstein-Barr virus
(responsible for Mononucleosis), and can be eliminated with a viral antibiotic
like acyclovir (Zovirax®), famciclovir (Famvir®) or valacyclovir
(Valtrex®). This condition is rarely seen in patients not infected
with HIV. However, some healthy patients may develop a
"callous" on the lateral borders of the tongue due to the
nervous habit of continually scraping the tongue over the teeth. This can
lead to embarrassment if the dentist suggests an AIDS test to a person who
believes such a suggestion is an insult! It is never meant as a value
judgment. Hairy Leukoplakia is not contagious. click the image to
see a larger version of this image and more information on hairy leukoplakia.
Herpes Zoster
(better known as shingles)
is caused by the same virus that causes Chicken Pox. Herpes
zoster "hides out" in a somatic nerve branch after the initial
Chicken Pox infection (which usually happens in childhood), and flares up again
later in life when the immune system begins to fail. Shingles is common
in otherwise healthy elderly persons. It generally does not occur in
younger people unless they are concurrently infected with the AIDS virus.
The distribution of the rash on the body is the key to the diagnosis of
shingles, and distinguishes the herpes zoster virus from other forms of herpes
viruses. The distribution of the rash caused by herpes zoster in shingles
is almost always on one
side of the body, and is
confined to the distribution of a single nerve root. The skin
surface distribution of each spinal or cranial nerve is called a dermatome. The
image on the left shows a rash which is confined to the dermatome defined by
the third branch of the trigeminal nerve. It is outlined in blue to make
it easier to see. Click the image to see larger images, as well as a
great deal more on the concept of somatic dermatomes. Shingles infections
are quite painful, and they generally go away after four or five weeks, but
shingles may reoccur again at a later date. It frequently leaves those so
afflicted with "postherpetic neuralgia" (PHN),
which is severely sensitive skin, well after the infection.
Persons infected
with HIV are prone to this disease if they have previously been infected with
Chicken Pox. For people with AIDS, this condition can be severe and even
life threatening. In the mouth, it is identified by its distribution. It
is limited to one side of the affected organ. The image to the right
shows the Herpes zoster virus infecting half of the upper posterior
palate. It is easy to confuse Herpes zoster with Herpes simplex which may
occur in the same distribution purely by chance. While the Herpes simplex
virus is contagious, Shingles, surprisingly is not. Since a large
percentage of the population already has been exposed to Chicken pox, most
people harbor an immunity to Herpes zoster, and the probability that anyone
will develop this disease depends more on the state of their immune system than
on recent exposure to the virus.
Herpes Simplex (the "cold sore" or "fever blister" virus)
Herpes
Simplex (type I) is the virus that
causes cold sores in normal, healthy adults. The image at the right
shows a typical cold sore, sometimes called a fever blister due to its
propensity to appear when the patient has a cold or other febrile (fever
causing) illness. This is another bug that, like Shingles, tends to "hang
out" in a nerve root for the life of the patient after the initial
infection, which often occurs in childhood. Once infected, the patient
remains infected for life. However the virus remains dormant inside
the nerve root most of the time until the patient suffers an illness or other
problem which lowers his immune response. The virus takes advantage of
the drop in immune response to flare up in the typical cold sore seen in this
image. Click the image above for more on Herpes simplex.
This image is what the initial infection may look like when a child, or
young adult is first infected with the Herpes Simplex
virus. This is called "Primary Herpes stomatitis",
and as you can see, it can look quite severe with blisters both inside and
outside the mouth. ("Stomatitis" means inflammation of the
entire mouth.) The patient is quite sick, but this primary infection will
disappear after 10-14 days with rest and lots of fluids. In healthy
people, this infection happens only once in a lifetime. The presence of
the virus only becomes apparent in adulthood whenever a cold sore
appears.
Whenever an adult
appears in a clinic with a case of Primary Herpes Stomatitis, this infers a
severely depressed immune response, and the dentist might consider referring
the patient to a physician for diagnosis of an underlying disorder. Adults
presenting with severe herpes stomatitis should consider being tested for
HIV. It must be remembered, however, that a primary herpes stomatitis can
happen at any time of life if the patient has never before had a cold
sore. Click on the
image to see larger views of this condition.
Patients with AIDS
have immune systems much more depressed than normal people with a cold or the
flu. AIDS victims may get not only recurrent cold sores, but recurrent
(repeating) cases of full blown Herpes Stomatitis as well. Whenever an
adult appears in a clinic with a case of Primary Herpes Stomatitis, this infers
a severely depressed immune response, and the treating physician or dentist may
suspect an undiagnosed HIV infection underlying the Herpes infection. New antibiotics
like acyclovir (Zovirax®), famciclovir (Famvir®) or valacyclovir (Valtrex®) are
effective in suppressing the Herpes.
Herpes simplex
blisters can sometimes occur in the oral cavity on tissues not generally
associated with cold sores. They alwayshappen
on tissue that is firmly bound down to underlying bone, such as the gums
immediately around the teeth or on the roof of the mouth. As you can see,
the appearance of this infection in the mouth can easily be confused with Herpes Zoster (shingles), especially if it occurs
on only one side of the mouth. The viruses are closely related, and the
blisters in the oral cavity can look identical.
The presence of
this type of infection in the mouth does not indicate the presence of HIV,
although this infection is more common in AIDS patients than in the non-HIV
population. This can happen to anyone who harbors the Herpes Simplex
virus. Left alone, provided the patient is not immunologically
compromised, it disappears in 10 to 14 days and may be treated with acyclovir
(Zovirax®), famciclovir (Famvir®) or valacyclovir (Valtrex®) for quicker
recovery. The herpes simplex virus is very contagious and if one
person in a family develops a cold sore, then others in the family may develop
one as well.
For more basic
information on the various forms herpes simplex takes, visit HerpesEductaion.Org.
Herpes Simplex type I (HSV-1) tends to infect the
face and oral cavity. This virus is the one responsible for traditional
cold sores, as well as primary herpes stomatitis. However, there is a
second variety of Herpes that prefers to infect the genital areas. Herpes
Simplex Type II (HSV-2) is called "genital Herpes"
because of its tendency to be transmitted sexually. Both HSV-1 and HSV-2
produce similar lesions. The difference between them is their site
specific preferences. Both varieties establish latency (in other words,
they take up permanent residence) in nerve roots and once established, tend to
cause occasional recurrent outbreaks with active lesions (sores) in areas of
the body serviced by that particular somatic nerve root. Herpes
Simplex type 1 prefers to live in thetrigeminal nerve root where it causes lesions in the mouth and on the face. HSV-2 takes
up residence in the sacral ganglion, located at the base of the spine, where it
may cause genital lesions (see the dermatome chart on the Herpes zoster page).
Even though each
type of Herpes virus has site specific preferences, they are genetically
similar, and can take up residence in nerve roots in other parts of the body, including in each other's
territory. However, outside of their own home territories
neither virus is especially virulent, and rarely cause recurrent
outbreaks.
HSV-2 (genital
herpes) causes approximately 90% of all cases of genital herpes
outbreaks. The other 10% is caused buy HSV-1. Genital herpes caused
by HSV-1 is generally much milder than that caused by HSV-2. HSV-1,
the "cold sore virus", is usually transferred to the genital
area by direct oral/genital contact, but upon occasion can be transferred from
a patient's mouth to their own genitals (or someone else's) by simple manual
transfer. Thus the use of saliva as a lubricant can transfer HSV-1 to the
genital area. Most people infected with HSV-1 in the genital area have few, if any,
outbreaks after the initial episode. HSV-2 prefers to live in this area
and causes a much more virulent infection there.
On the other hand,
HSV-1 causes almost all cases of oral and facial herpes. Oral herpes
caused by HSV-2 is not likely to cause recurrent infections, except in
immunocompromised patients.
Warts are caused
by a virus. In the oral cavity, they tend to be somewhat flatter than the
type occurring on hands, but if they are dried with air, the tiny projections
characteristic of regular warts become evident. The causative agent is
the Human Papillomavirus (HPV). These growths generally are not painful
and can be ignored unless they interfere with appearance or function.
Persons infected with HIV may develop very large, multiple warts. They
may be removed using lasers, cautery or cold steel blades. The presence
of oral warts is not in itself an indication of
AIDS, although some strains of the virus are associated with squamous cell
carcinoma (oral cancer). HPV is contagious. Click on the image
for more information on HPV and its association with oral and cervical cancer
Kaposi's Sarcoma
is a form of cancer consisting of an overgrowth of tiny blood
vessels. It is generally dark red or deep purple. It may be flat,
but sometimes presents as a swollen mass. The lesions are rarely painful,
unless they become secondarily infected. Thus good oral hygiene is
important in the management of these tumors when they occur in the mouth.
Kaposi's Sarcoma is most frequently seen on the skin. However
tumors can occur in the gastrointestinal tract and the oral cavity as
well. Lesions in the oral cavity occur mostly on the palate (the roof of
the mouth). Kaposi's is technically a form of cancer, however there
is evidence that it is actually the result of a secondary infection with Herpes
virus type VIII. An abundance of this virus is found in the saliva of
infected individuals. However, the virus causes Kaposi's Sarcoma
only in patients with very compromised immune systems. It is believed
that in most
modern cases,
Herpes virus type VIII is transferred through deep kissing.
Kaposi's tumors
were once seen exclusively in elderly men with compromised immune
systems. Today, however, they are seen more frequently in young men with
AIDS. The occurrence of one of these lesions anywhere on the body of a young man isindicative
of the presence of HIV. Kaposi's is rarely seen in women, even women infected
with HIV. It is also rarely found in men who have contracted AIDS by way
of intravenous drug use. It is not known why women and heterosexual males with AIDS do not generally get
Kaposi's sarcoma, although there is probably an association between the gay
lifestyle and the transfer of the herpes type VIII virus. Kaposi's occurs as
the initial manifestation of AIDS in approximately 11% of patients.
Non Hodgkin's
Lymphoma (NHL) is a form of cancer. It starts in a lymph node and
then spreads to other areas of the body through the blood vessels
and the lymphatic system. Before the era of AIDS, Non Hodgkin's lymphoma
usually affected older individuals (median age 67). Unfortunately, since
the beginning of the AIDS epidemic the incidence of NHL has increased
substantially in younger persons. Lesions like those in the image to the
right, especially when present in a younger person, may be the first indication
that a patient has an HIV infection. NHL is usually accompanied by
a generalized lymphadenopathy (generalized swelling of the lymph
nodes). However, persons with no history of immunosuppression (or
HIV) may contract the disease. Click the image for more
information on this condition and its relation to HIV.
In order to
understand how periodontal disease (gum disease) affects persons with
AIDS, it will be helpful to read my explanation ofregular periodontal disease, since the process in HIV infected people is the same (albeit more severe
and much more rapidly progressing) as in otherwise healthy people.
The treatment for HIV infected persons is also the same as the treatment for otherwise healthy persons with
Periodontal disease, except that irrigation with Betadine (an Iodine
solution) and more aggressive antibiotics are used.
In light of the
fact that Gum Disease in HIV infected patients is so similar to the variety
seen in the normal population, it is unlikely that a dentist would draw a
parallel between the presence of this process and the presence of HIV
until the condition presented itself like the picture below and to the right.
The image to the
right shows a case of necrotizing
ulcerative periodontitis.
The difference between periodontitis and gingivitis is the degree of bony involvement and the depth of the pocketing. The white, red and bleedy area under the necks of the lower
teeth is indicative of necrotizing (in the process of dying) tissue.
While the process can be halted by aggressive intervention from a dentist and
periodontal health maintained by good oral hygiene, the damage to the gums and
bone is permanent. Periodontal disease is caused by poor oral hygiene and is
not contagious.
A less severe form
of this condition found in the non HIV infected population (also seen in early stages
of AIDS) is called Acute
Necrotizing Ulcerative Gingivitis (ANUG), formerly called "Trench
mouth". In ANUG, only the gingiva immediately
surrounding the teeth becomes necrotic. ANUG is often found in people
with poor oral hygiene who are either ill or under extreme
physical or emotional stress. (It was named "trench mouth" because it
was common in soldiers who fought in the trenches during world war I.
These men were certainly under extreme physical and emotional stress, and had
little opportunity to brush their teeth.)
ANUG, being a
bacterial infection, is very easily treated by gentle cleaning of the teeth and
irrigation of the affected gums with 3% hydrogen peroxide. The bacteria
that take advantage of a patient's run-down condition tend to be anaerobic
which means that they die in the presence of oxygen. Hydrogen peroxide
liberates oxygen (hence the bubbles) when it is exposed to blood, and the
oxygen acts as an antiseptic and speeds healing of the damaged gum
tissue. The patient is sent home with a prescription for Penicillin and
instructions on cleaning
the teeth to prevent further problems.
ANUG is not contagious.
Dentists today
rarely see cases of ANUG, however the disease is making a comeback in
communities in which there is a lot of drug addiction. It is especially
prevalent in populations of methamphetamine addicts and is a part of the
syndrome now known as Meth
Mouth.
This condition is
never seen except in a hospital setting. If the immune system is severely
compromised, the body is unable to fight off bacterial infections that a normal
immune system is able to combat easily. Without a functioning immune system,
normal environmental bacteria can attack a living body in the same way they
would attack a dead body. HIV attacks the immune system, immobilizing
it. Without a properly functioning immune system, there is no defense
against parasitic bacteria and viruses, and a living body can start to decay.
Other indications of immune deficiency
Geographic
tongue--This condition is thought to be an
oral form of psoriasis (a common skin condition), and is characterized by the
disappearance of the filiform
papillae from irregular patches on the top
surface of the tongue. These patches then "heal" up and reoccur
on another part of the tongue at a later date. One can see lesions in
varying stages of healing over large expanses of the tongue. The cause of
this condition is unknown. These patients often complain of pain when
eating sharp foods. The condition can be treated with topical application
of steroid gels or mouth rinses. In general, however, it is not
treated. Geographic tongue is not a contagious condition. This
condition might be seen more frequently in AIDS
patients, however the presence of geographic tongue does NOT mean that the patient
has AIDS. It may be more prevalent in persons with HIV because the virus
attacks the immune system, and psoriasis is caused by a mal fun ti on of the
immune system. Click the image on the right for a larger view.
Syphilis
Prevention and Treatment
Syphilis is a sexually transmitted disease (STD), once responsible for
devastating epidemics. It is caused by a bacterium called Treponema pallidum.
The rate of primary and secondary syphilis in the United States declined by
89.2 percent from 1990 to 2000. The number of cases rose, however, from 5,979 in 2000 to 6,103 in 2001. The U.S. Centers for Disease
Control and Prevention reported in November 2002 that this was the first
increase since 1990.
Of increasing concern is
the fact that syphilis increases by 3- to 5-fold the risk of transmitting and
acquiring HIV (human immunodeficiency virus), the virus that causes AIDS
(acquired immunodeficiency syndrome).
The syphilis bacterium is very fragile, and the infection is almost
always transmitted by sexual contact with an infected person. The bacterium
spreads from the initial ulcer (sore) of an infected person to the skin or
mucous membranes (linings) of the genital area, mouth, or anus of an uninfected
sexual partner. It also can pass through broken skin on other parts of the
body.
In addition, a pregnant
woman with syphilis can pass T. pallidum to her unborn child, who may be born
with serious mental and physical problems as a result of this infection.
The initial infection causes an ulcer at the site of infection. The
bacteria, however, move throughout the body, damaging many organs over time.
Medical experts describe the course of the disease by dividing it into four
stages-primary, secondary, latent, and tertiary (late). An infected person who
has not been treated may infect others during the first two stages, which
usually last 1 to 2 years. In its late stages, untreated syphilis, although not
contagious, can cause serious heart abnormalities, mental disorders, blindness,
other neurologic problems, and death.
Primary Syphilis
The first symptom of
primary syphilis is an ulcer called a chancre ("shan-ker"). The
chancre can appear within 10 days to 3 months after exposure, but it generally
appears within 2 to 6 weeks. Because the chancre may be painless and may occur
inside the body, the infected person might not notice it. It usually is found
on the part of the body exposed to the infected partner's ulcer, such as the
penis, vulva, or vagina. A chancre also can develop on the cervix, tongue,
lips, or other parts of the body. The chancre disappears within a few weeks
whether or not a person is treated. If not treated during the primary stage,
about one-third of people will go on to the chronic stages.
Secondary syphilis
A skin rash, with brown
sores about the size of a penny, often marks this chronic stage of syphilis.
The rash appears anywhere from 3 to 6 weeks after the chancre appears. While
the rash may cover the whole body or appear only in a few areas, it is almost
always on the palms of the hands and soles of the feet.
Because active bacteria
are present in the sores, any physical contact-sexual or nonsexual-with the
broken skin of an infected person may spread the infection at this stage. The
rash usually heals within several weeks or months.
Other symptoms also may
occur, such as mild fever, fatigue, headache, sore throat, patchy hair loss,
and swollen lymph glands throughout the body. These symptoms may be very mild
and, like the chancre of primary syphilis, will disappear without treatment.
The signs of secondary syphilis may come and go over the next 1 to 2 years of
the disease.
Latent syphilis
If untreated, syphilis
may lapse into a latent stage during which the disease is no longer contagious
and no symptoms are present. Many people who are not treated will suffer from
no further signs and symptoms of the disease.
Tertiary syphilis
Approximately one-third
of people who have had secondary syphilis go on to develop the complications of
late, or tertiary, syphilis, in which the bacteria damage the heart, eyes,
brain, nervous system, bones, joints, or almost any other part of the body.
This stage can last for years, or even for decades. Late syphilis can result in
mental illness, blindness, other neurologic problems, heart disease, and death.
Syphilis is sometimes called "the great imitator" because its
early symptoms are similar to those of many other diseases. Sexually active
people should consult a doctor or other health care worker about any rash or
sore in the genital area. Those who have been treated for another STD, such as gonorrhea, should be tested to be sure they do not also have syphilis.
There are three ways to
diagnose syphilis.
The doctor usually
uses all these approaches to diagnose syphilis and decide upon the stage of
infection.
Blood tests also provide
evidence of infection, although they may give false-negative results (not show
signs of an infection despite its presence) for up to 3 months after infection.
False-positive tests (showing signs of an infection when it is not present) also
can occur. Therefore, two blood tests are usually used. Interpretation of blood
tests for syphilis can be difficult, and repeated tests are sometimes necessary
to confirm the diagnosis.
Unfortunately, the early symptoms of syphilis can be very mild, and many
people do not seek treatment when they first become infected.
Doctors usually treat
patients with syphilis with penicillin, given by injection. They use other
antibiotics for patients allergic to penicillin. A person usually can no longer
transmit syphilis 24 hours after starting treatment. Some people, however, do
not respond to the usual doses of penicillin. Therefore, it is important that
people being treated for syphilis have periodic blood tests to check that the
infectious agent has been completely destroyed.
People with neurosyphilis
may need to be retested for up to 2 years after treatment. In all stages of
syphilis, proper treatment will cure the disease. But in late syphilis, damage
already done to body organs cannot be reversed.
A pregnant woman with untreated, active syphilis is likely to pass the
infection to her unborn child. In addition, miscarriage may occur in as many as
25 to 50 percent of women acutely infected with syphilis during pregnancy.
Between 40 to 70 percent of women with active syphilis will give birth to a
syphilis-infected infant.
Some infants with
congenital syphilis may have symptoms at birth, but most develop symptoms
between 2 weeks and 3 months later.These symptoms may include
People who care
for infants with congenital syphilis must use special cautions because the
moist sores are infectious.
Rarely, the symptoms of
syphilis go undetected in infants. As infected infants become older children
and teenagers, they may develop the symptoms of late-stage syphilis, including
damage to their bones, teeth, eyes, ears, and brains.
Syphilis bacteria frequently invade the nervous system during the early
stages of infection. Approximately 3 to 7 percent of persons with untreated
syphilis develop neurosyphilis, a sometimes serious disorder of the nervous
system. In some instances, the time from infection to developing neurosyphilis
may be up to 20 years.
Some people with
neurosyphilis never develop any symptoms. Others may have headache, stiff neck,
and fever that result from an inflammation of the lining of the brain. Some
people develop seizures. People whose blood vessels are affected may develop
symptoms of stroke with numbness, weakness, or visual problems. Neurosyphilis
may be more difficult to treat, and its course may be different, in people with
HIV infection or AIDS.
The open sores of syphilis may be visible and infectious during the
active stages of infection. Any contact with these infectious sores and other
infected tissues and body fluids must be avoided to prevent spread of the
disease. As with many other STDs, using latex male condoms properly during
sexual intercourse may give some protection from the disease.
Screening and treatment
of infected individuals, or secondary prevention, is one of the few options for
preventing the advanced stages of the disease. Testing and treatment early in
pregnancy are the best ways to prevent syphilis in infants and should be a
routine part of prenatal care.
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