Indications for cardiac surgery in Infective Endocarditis:

đź”… Heart Failure due to valve damage
đź”… Failure of antibiotic therapy
đź”… Large vegetations
đź”… Abscess formation

Dr. Mehnaz Memonđź–Š

References: Davidson’s Principles and Practice of Medicine Textbook


When a bacterium is inoculated into a suitable culture medium and is incubated, growth takes place and follows a definite course.

The bacterial growth count is plotted in relation to time , hence growth curve is obtained.

It has 4 phases .

  1. Lag phase
  2. Log phase / exponential phase
  3. Stationary phase
  4. Phase of decline

So let’s know what are these phases

1. Lag phase –

•after inoculation of culture medium multiplication does not begin immediately.

•the phase between inoculation and beginning of multiplication is called as lag phase

•in this phase organisms adapt to the new environment, in which necessary enzymes and intermediate metabolites are built up .

2. Log phase (exponential phase )

•in this phase cell division starts and the number increases exponentially or by geometric progression.

3. Stationary phase

•bacterial growth ceases almost completely.

•almost complete exhaustion of nutrients and accumulation of toxic products takes place.

•the number of viable cells here remain stationary.

Also there is almost a balance between dying cells and the new formed cells.

4. Phase of decline

• the bacterial population decreases due to death of cells.

•the decline phase starts due to exhaustion of nutrients and accumulation of toxic products and autolytic enzymes.

Decline takes place in the viable count and not the total count.


bacterial count-

It’s of two types

1. Total count- indicates total number of bacteria present in the specimen, irrespective of living or dead.

2. Viable count- number of living cells.

To summarise it

Source – C P Baveja ( textbook of microbiology for dental students)

Mycobacterium tuberculosis Infection


  • Obligate human pathogen.
  • Approximately 1/3 of the world population is infected, and there are 8-10 million new cases each year.
    – Of these, 5-10% will develop tuberculosis disease, which kills 1-4 million people annually.
  • Individuals with HIV or other immune deficiencies are more likely to develop severe infection; because of this, co-infection with HIV and tuberculosis is a major public health concern in areas where both infections are endemic.
  • Transmitted from human to human via respiratory aerosols
  • Microbes are inhaled and travel to the lungs, where they are engulfed by alveolar phagocytes.
  • Mycobacterium tuberculosis has evolved to highjack the innate immune response and to delay the adaptive immune response.
    – Disease development is the outcome of host and bacterial interactions that produces chronic inflammation.

Primary infection

  • Occurs when a new host first encounters Mycobacterium tuberculosis
  • Alveolar macrophages engulf Mycobacterium tuberculosisbacteria and sequesters the bacteria within a vacuole.
    – Recall that part of the innate immune response involves phagocytosis of microbes, followed by phago-lysosome fusion to expose the microbes to bactericidal lysozymes.
  • Mycobacterium tuberculosis prevents phago-lysosome fusion,thus evading destructive enzymes.
    – Allows fusion with nutrient-filled vesicle to facilitates its own replication within the macrophage.
  • Infected macrophage responds by secreting IL-12 and Tumor Necrosis Factor alpha (TNF-alpha).
  • These cytokines recruit other immune cells to the area:
    – Natural killer cells, CD4+ T cells, and Monocytes.
  • The CD4+ T cells differentiate to become Helper T cells that release Interferon gamma, which is a cytokine that activates macrophages.
    – Interferon gamma triggers the following antibacterial effects: Phagolysosome maturation, production of oxygen reactive species and nitric oxide, antimicrobial defensin recruitment, autophagy, and macrophage differentiation to form epithelioid cells.
    – Not surprisingly, patients with low production of TNF-alpha and/or interferon-gamma are more susceptible to severe Mycobacterium tuberculosis infection.
  • Macrophage activation and the other effects of interferon-gamma promotes intracellular killing.
  • Mycobacterium tuberculosis can induce macrophage apoptosis to escape killing.
  • The monocytes recruited by IL-12 and TNF can also be infected; thus, instead of fighting bacterial spread, the newly arrived monocytes promote its success.
  • The host’s response to Primary infection leads to chronic inflammation and granuloma formation.

Chronic inflammation produces granulomas, aka, tubercles

  • Granulomas are hallmarks of primary tuberculosis infection that reflect interactions between the adaptive immune response and invading bacteria.
  • They comprise aggregations of immune cells that wall-off bacteria in areas of the lungs and lymph nodes.
    – Necrotic center comprises apoptotic macrophages and Mycobacterium tuberculosis.
    – Center is surrounded by layers of epithelioid macrophages and Langhans giant cells (fused epithelioid cells).
    – B-cells, T-cells, and neutrophils also surround the necrotic center.
    – Outer fibrous layer encircles the granuloma.
  • In a histological sample of infected lung tissue, we can see multiple granulomas with caseous (“cheese-like”) necrotic centers. Compare these areas with the remaining alveolar tissue, and consider how granulomas interfere with gas exchange in the lungs.
  • Primary tuberculosis infection is typically characterized by lesions in the lower lobes of the lung (Ghon foci) and in the hilar lymph nodes, which drain the lungs.
    – Collectively, the pulmonary and lymph node lesions are referred to as the Ghon complex.
  • The Ghon complex can calcify and become a fibrotic Ranke complex, which reflects latent infection.
    – Early studies stressed the benefits of granuloma formation to the host – bacterial spread is prevented by layers of host tissues. However, we now recognize that those layers of cells also prevent the host immune system or clinical therapies from reaching the bacteria, which allows infection to persist in a dormant state.
    – Ultimately, the dormant bacteria can reactivate to cause secondary infection.

Secondary infection

  • Tuberculosis infection in an individual who has previously been exposed to Mycobacterium tuberculosis
  • Occurs upon reactivation of dormant bacteria or re-infectionfrom a new source.
  • Secondary infection is characterized by lesions in the upper lobes of the lungs and does not involve the lymph nodes (in contrast to primary infection lesions).
  • Many lesions heal spontaneously, and can leave behind fibrotic scars.
  • Others lead to caseation and cavitation.
    – Bacteria replicate within the lesions and are released in sputum along with fragments of necrotic lung tissue.
    – The contaminated sputum constitutes the is the primary route of Mycobacterium tuberculosis transmission between humans.

Hematogenous spread of Mycobacterium tuberculosis

  • Occurs in primary or secondary pulmonary infections.
  • It is especially likely in individuals with impaired cellular immunity.
  • Miliary tuberculosis occurs when the resulting lesions are very tiny (like millet seeds); infection can by systematic or localized within a specific organ.
  • Isolated tuberculosis with larger lesions can also occur.
  • Extrapulmonary infections can occur in any organ, but are particularly common in the liver, spleen, kidney, adrenal glands, bone marrow, lymph nodes, and the meninges.

Prevention and treatment

  • Bacille Calmette-Guerin (BCG) vaccine is administered to children in areas where tuberculosis is endemic.
    – Vaccine is made with attenuated Mycobacterium bovis.
    – Significant limitations: it is only effective against some forms of childhood tuberculosis, and is not effective against pulmonary tuberculosis, which is the most prevalent form of the disease.
  • Skin and blood tests can determine if Mycobacterium tuberculosis is present in the body.
    – These tests do not distinguish between latent and active infections; individuals who’ve had the Mycobacterium bovis vaccine will test positive.
  • Chest x-rays can show cavitation and pulmonary tissue damage.
  • Mycobacterium tuberculosis is resistant to antibiotics
    – Long-term, multi-drug therapy is necessary.
    – “Extensively drug-resistant” strains (XDR TB) are on the rise in some regions.