Tuberculosis : in man and animal

Tuberculosis

Tuberculosis is a chronic granulomatous disease of man and animal. Older animals show more clinical disease. It usually involves the lungs but may affect any organ or tissues of the body.

Causal Agent: Mycobacterium species. Myco means wax or fungus. These bacteria are –

v Aerobic

v Acid fast

v Facultative intracellular bacteria

v Large rod shaped bacteria

In 1882 Robert Koch discovered this bacterium. So the bacterium is also known as Koach`s bacillus.

Species and disease (Mycobacterium)

Species Host Disease
1.M. tuberculosis Human, others Tuberculosis
2. M.bovis Human, cattle Tuberculosis/bovine tuberculosis
3. M.paratuberculosis Cattle John’s disease/chronic bacillary dysentery
4.M.ovium Domestic & wild birds Avian tuberculosis
5.M.laprae Human Leprosy

 

Why Acid Fast?

The cell wall composed of peptidoglycan, lipid, mycolic acids, cord factor and wax- D. Due to waxy coat when the bacteria is heated with the primary stain carbol fuchsin, the lipid rich layer becomes permeable to allow the stain within it. But when heating is closed the cell wall again becomes hardy and does not allow the distaining acid alcohol to enter to distain carbol fuchsin. Due to this impermeability to distaining acidic solution, this is called acid-fast organism.

What is granulomatous disease?

Any chronic inflammatory infiltrate composed predominantly of macrophages is called granulomatous disease.

A granuloma is focally discrete chronic inflammatory reaction composed predominantly but not exclusively of macrophages.

In the granuloma the macrophages must be organized or aggregated is closely packed collections or sheath and they are in activated stages that mean those macrophages are more efficient for killing microorganisms and more productive for cytokines and degenerative enzymes.

 

How T cells contribute to defense against tuberculosis?

T cell contribute to defense against infections by producing specific patterns of cytokines, which can be broadly divided into type 1 cytokines including interferon- γ,interferon 2, IL-2, IL-12, IL-18 and type 2cytokines, including IL-4 and IL-5, IL-10 and TGF-β. Interferon γ contributes to protective immunity against Mycobacterium by activating macrophages to more effectively eliminate these organisms. IL-12 and IL-18 are macrophage products that strongly favor development of type 1 cytokine response. T cells medicate immune defenses against Mycobacterium tuberculosis is essential and interferon γ is critical for protective immunity.

Pathogenesis:

Organism enters into body by any route.

First defense cell neutrophil attacks and try to engulf and destroy bacteria but failed.

Multiplication of organism with in neutrophils.

 

Destruction of neutrophils.

 

Dead neutrophils stimulate the accumulation of macrophages.

 

With few hours macrophages try to phagocytise the bacteria but it fails to destroy because acid fast bacteria contain glycolipid.

Then microorganism multiplies within macrophage.

 

Macrophage modified into epitheloid cell (secretory function).

 

Organism come contact into epitheloid cell.

It also fail to destroy organism.

 

Bacteria multiply and come to the periphery.

Then epitheloid cell to form giant cell.

Various types of giant cell found specially langhan`s type giant cell.

 

Giant cell engulf bacteria.

If giant cell failed then proliferation of fibroblast cell occur.

Then fibrin network produce where encapsulated the organism.

Formation of nodule.

Coalensence of two nodules form a large nodule.

What is epitheloid cell?

Epitheloid cells are modified macrophages in the granuloma which have abundant finely granular eosinophilic cytoplasm, vesicular nuclei and indistinct cell boundary similar to an epithelial cell. These cells have rich endoplasmic reticulum and golgi bodies indicating specialized for biosynthesis of protein (e.g. cytokine and enzymes) rather then phagocytosis and killing.

 

Gross appearance:

v Firm/ hard, white gray or yellow nodule.

v On cut section it`s yellowish, caseous, necrotic center is dry and solid contrast to the pus in an abscess.

v Calcification is common in many animals and sectioning with a knife a gnitfy sensation grating sound will appear occasionally a tubercle breaks into a blood vessels the bacilli the lodge in capillaries of the parenchymatous organs (liver, kidney, spleen) where they give rise to same age and size (2-3 mm in diameter) of tubercle those looks like that of millet seed. It is called military tuberculosis.

 

Lesions in different species:

v In bovine calcification is often prominent particularly in lymph node. The dissiminated tubercles (0.5- 1.0 cm in diameter) over the pleural and peritoneal surfaces are also fairly common. These tubercles look like of pearl and so called pearl disease.

v In horse, the lesions are usually rarely exhibit caseation and calcification and alimentary infection is the usual form.

v In birds calcification is seldom observed.

v In swine, tuberculosis caused by avian type appears as multiple caseocalcarious encapsulated foci, most often affecting lympf nodes of the head and neck mesenteric lymph nodes and intestinal mucosa.

v In non human primates, the disease is usually pulmonary and milliary lesions are frequent caseation is often prominent and calcification is rare.

Transmission:

Organisms are excreted from infected animal through exhaled sputum/ saliva/ cough, feces, milk, urine, vaginal and uterine discharges, nasal discharges. Transmission occurs both vertically and horizontally. Horizontal transmission occur both directly and indirectly and indirectly.

Sample collection:

v Samples for tuberculosis include: Cough, sputum incase of respiratory form of disease, feces incase of alimentary form and milk in case of tuberculous mastitis.

v Samples from dead animal: Tubercle is incised and caseous mas in collection.

v Sample from birds: Avian tuberculosis is characterized by occurrence of irregular grayish- yellow or grayish- white nodules of varying size un organ if predilection such as- spleen, liver, intestine.

v Samples from human: Sputum, cough, stool etc.

 

Clinical Signs:

Clinical disease is often looking even in advanced stage disease. Clinical disease depends upon the extant and location of disease.

  1. Progressive emaciation, lethargy, anorexia, fluctuating fever.
  2. Respiratory form of disease: Intermittent and moist cough with later stage of dyspneaq and tachypnea.
  3. Alimentary form: Intermittent diarrhea, bloat.
  4. Tuberculous mastitis: A hard pain less enlargement of udder with physical change of milk.
  5. The course of the disease varies greatly monyhs to years even one may not show clinical disease in its life span.

Clinical sign in human: Fever, night- time sweating, loss of weight, persistent cough, loss of appetite.

Dignosis:

  1. In living animals the diagnosis based on X- rays findings, tuberculin test and demonstration of organisms in exudates or secretion.
  2. Histopathological lesions demonstration of acid fast organisms within typical tubercles.
  3. Isolation and identification of organisms.

 

 

 

লেখকঃ ডা মোঃ মুস্তাফিজুর রহমান পাপ্পু

ডা মোঃ মুস্তাফিজুর রহমান পাপ্পু
I am Kbd Dr.Md.Mustafijur Rahaman Pappu. I have completed Doctor of Veterinary Medicine (DVM) Degree and Master's in Pathology under Faculty of animal science & veterinary medicine of PATUAKHALI SCIENCE & TECHNOLOGY UNIVERSITY( PSTU) My home town is JHENAIDAH . কৃষিবিদ ডা মোঃ মুস্তাফিজুর রহমান পাপ্পু যুগ্ম সাধারন সম্পাদক, বাংলাদেশ ভেটেরিনারি এসোসিয়েশন (বিভিএ),খুলনা বিভাগ। কার্যনির্বাহী সদস্য, বঙ্গবন্ধু ভেটেরিনারি পরিষদ, কেন্দ্রীয় কমিটি। সাবেক প্রতিষ্ঠাতা সাধারন সম্পাদক, ভেটেরিনারি স্টুডেন্টস এসোসিয়েশন (ভিএসএ),পবিপ্রবি। সাবেক সহ সভাপতি , বাংলাদেশ ছাত্রলীগ, পবিপ্রবি শাখা। Mobile -01915 084474. 01771 444402

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    dr. k.m. ehasanul islam(Rinto)

    Thanks Pappu. CARRY on………………..

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