1. By Dr.Sujith S

2. Species
Mycoplasma pneumoniae
Mycoplasma hominis
Mycoplasma genitalium
Ureaplasma urealyticum

3. Pathogenesis
Pathogenic organisms for humans and animals
possess specialized tip organelles that mediate their
interactions with host cells.
This host-adapted survival is achieved by i)surface
parasitism of target cells
ii) the acquisition of essential biosynthetic precursors
iii) cell entry and intracellular survival.

4. Toll-like receptor 2 for binding of Mycoplasma and
activation of inflammatory mediators, including
cytokines.
M. pneumoniae grows under both aerobic and
anaerobic conditions ,isolated on media
supplemented with serum.
The organism most commonly exists in a filamentous
form and has adherence proteins that attach to
epithelial membranes with particular affinity for
respiratory tract epithelium

5. An immune-mediated mechanism in infants and
young children developing pneumonia.
In addition, the antibodies produced against the
glycolipid antigens of M. pneumoniae may act as
autoantibodies, since they crossreact with human red
cells and brain cells.

6. Epidemiology
M. pneumoniae is transmitted from person-to-person
by infected respiratory droplets during close contact.
The incubation period after exposure averages three
weeks .
Infection occurs most frequently during the fall and
winter but may develop year-round

7. Mycoplasma pneumoniaeone of the most common
causes of atypical pneumonia
Atypical pneumonia  account for 7 to 20% of
community-acquired pneumonia
The incidence may be higher in patients with milder
disease that can be managed without hospitalization

8. Many infections due to M. pneumoniae are
asymptomatic.
The signs and symptoms vary according to the stage
of illness
Headache, malaise, and low grade fever.
Chills are frequent.

9. Cough due to M. pneumoniae infection ranges from
nonproductive to mildly productive, with sputum
discoloration occurring late in the disease.
Wheezing may occur
Pharyngitis
Rhinorrhea and
Ear pain

10. Extrapulmonary manifestations
These manifestations include
Hemolysis
Skin rash
Joint involvement
Symptoms and signs indicative of gastrointestinal tract,
central nervous system, and heart disease..

11. Haemolysis
Antibodies (IgM)  I antigen on erythrocyte
membranes appear during the course ; produce a cold
agglutinin response in about 60 % of patients .

12. Skin Disease
Dermatologic manifestations a mild erythematous
maculopapular / vesicular rash to the Stevens-
Johnson syndrome.
16 % patients with Stevens-Johnson syndrome had
evidence of mycoplasma infection.

13. Central Nervous
System
CNS involvement occurs most frequently in children,
with encephalitis as the most frequent manifestation.
Other manifestations include aseptic meningitis,
peripheral neuropathy, transverse myelitis, cranial
nerve palsies and cerebellar ataxia .
Acute transverse myelitis (ATM) and acute
disseminated encephalomyelitis (ADEM) most
severe complications .
59 percent of patients presenting with spinal cord
involvement suffered permanent neurologic
sequelae .

14. Other Systems
Rheumatologic symptoms including tender joints
and muscles and polyarthritis.
Arthritis is believed to result from immune-mediated
mechanisms
M. pneumoniae has been isolated from synovial fluid
in some patients with polyarthritis.

15. Cardiac or renal involvement -unusual .
Rhythm disturbances, congestive heart failure, chest
pain, and conduction abnormalities on the
electrocardiogram.
Clinically significant glomerulonephritis is a rare
complication that is presumed to be secondary to
immune complex deposition

16. Chest X-Ray
Bronchopneumonia
Plate-like atelectasis
Nodular infiltration
Hilar adenopathy
The most common radiographic finding is the
peribronchial pneumonia pattern, which consists of a
thickened bronchial shadow, streaks of interstitial
infiltration, and areas of atelectasis; these changes have a
predilection for the lower lobes.
Nodular infiltrates and hilar adenopathy  less common,
and result in a broader differential diagnosis, including
tuberculosis, mycotic infections, and sarcoidosis

17. Lab Diagnosis
Subclinical evidence of hemolytic anemia is present
in the majority of patients with pneumonia positive
Coombs' test and elevated reticulocyte count.
Cold agglutinin titers are elevated in 50 percent of
patients with mycoplasma disease, and the titer
usually exceeds 1:128 in patients with pneumonia
With overt hemolysis, titers may be as high as
1:50,000.

18. Elevated Cold Agglutinin Titres
Infectious Mononucleosis secondary to Epstein Barr
virus
Cytomegalovirus
Adenovirus pneumonia
Viral illness
Lymphoma and Collagen vascular disorders

19. The white blood cell count (WBC) normal  75 to
90 percent of cases.
Thrombocytosis can occur acute phase response.

20. CSF-Lymphocytic pleocytosis, elevated protein, and
normal glucose.
Isolation of M. pneumoniae in CSF - possible.
A culture is more likely to be positive in encephalitis
rather than myelitis.
PCR testing for Mycoplasma in the CSF can also be
performed.

21. Treatment
Treatment options for outpatient community-
acquired pneumonia are presented in the 2007
consensus IDSA/ATS guideline:
Macrolide antibiotics (azithromycin,
clarithromycinor erythromycin) first line
treatment .
Azithromycin (500 mg orally once daily, initially
followed by 250 mg orally for 4 days) has become the
most commonly used drug regimen.

22. Adjunctive Therapy
For hemolytic anemia, case reports indicate some
patients respond to warming, steroid therapy,
possibly plasmapheresis.
For CNS disease, therapy with steroids,
antiinflammatory drugs, diuretics, and plasma
exchange ,used in addition to antibiotics.

23. M.Hominis
Epidemiology:M. hominis is part of the normal
genital flora of many sexually experienced men and
women
Infants & childrren:Newborns are likely to become
colonized during passage through the birth canal..

24. The organism
Mycoplasma are the smallest free-living bacteria. M.
hominis cannot be visualized by Gram stain.
M. Hominisproduces nonhemolytic colonies on
sheep blood agar after three to five days of
incubation.
M. hominis does not alter the appearance of blood
culture media; therefore,routine blind subculturing
onto blood is required for detection.

25. For optimizing the recovery of M. hominis, clinical
specimens should be immediately inoculated onto
culture media and not allowed to dry.
After plating, cultures should be promptly incubated
or kept at 4ºC.
The best laboratory culture media is beef heart
infusion broth (also known as pleuropneumonia-like
organism) (PPLO) broth with fresh yeast extract and
horse serum.

26. PCR is superior to traditional culture methods for
detecting M. hominis in genital secretions.

27. Genitourinary infection
Pyelonephritis
Pelvic inflammatory disease
Chorioamnionitis
Postpartum and postabortal fever
Nongenitourinary infections that have been linked to M. hominis
include:
Septicemia
Wound infections
Central nervous infections
Joint infections
Lower respiratory tract infections
Endocarditis

28. Post partum & post abortal fever
M. hominis causes approximately 10 percent of all
cases of postpartum and postabortal fever.
There was a fourfold rise in antibody titers in one-half
of all women who had postabortal fever compared to
only 2 of 53 controls who had abortion without fever.

29. PID
M. hominis was isolated from 4 of 50 fluid samples
taken directly from the fallopian tubes of women with
salpingitis.
Significant rises in antibody titers to M. hominis
occurred in 9 of 16 women with salpingitis who had
positive lower genital tract cultures for M. hominis .

30. UTI
M. hominis can frequently be recovered from the
lower genitourinary tract in men and women.

31. Chorioamnionitis
M. hominis, along with Ureaplasma urealyticum, is
frequently found in the amniotic fluid of women with
i)preterm labor,
ii) preterm premature rupture of
membranes
iii) spontaneous labor at term
iv) premature rupture of membranes at
term
v) chorioamnionitis

32. CNS
M. hominis infection has been associated with non-
functioning CNS shunts , brain abscess , subdural
empyema, and meningitis.
M. hominis arthritis can occur in women after childbirth,
in conjunction with congenital immune defects, such as
hypogammaglobulinemia , in association with
immunosuppression (eg, in solid organ transplant
patients) or lymphoma , or following joint replacement
surgery or trauma.
M. hominis arthritis is usually characterized by fever,
leukocytosis, and a purulent joint effusion with large
numbers of polymorphonuclear cells but a negative Gram
stain.

33. Wound infections
M. hominis has been associated with infected pelvic
hematoma , infected cesarean wounds, and sternal
wound infections

34. Treatment
Tetracycline is the treatment of choice

35. Thank you