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♨️ Spread by Oral/Fecal Route
(Infections may be spread by oral sex.)

✔️ Salmonella
✔️ Shigella
✔️ Campylobacter
✔️ Vibrio
✔️ Yersinia enterocolitica
✔️ Yersinia pseudotuberculosis
✔️ Bacillus cereus
✔️ Clostridium
✔️ Staphylococcus (also other routes commonly)
✔️ Enteroviruses, including poliovirus
✔️ Rotavirus
✔️ Norwalk agent
✔️ Hepatitis A
✔️ Toxoplasma—cat feces
✔️ Entamoeba
✔️ Giardia
✔️ All nematodes except filaria and Trichinella
✔️ All cestodes.


https://www.tg-me.com/general_laboratory_information
♨️ Contact: (Person-to-Person) Nonsexual

✔️ Impetigo (Strep and Staph)
✔️ Staphylococcus
✔️ Herpes I
✔️ Epstein-Barr (kissing)
✔️ Hepatitis B (all body fluids)
✔️ Molluscum contagiosum (wrestling teams).

https://www.tg-me.com/general_laboratory_information
💢 LABORATORY DIAGNOSIS
♨️ Special Stains

⭕️ Silver stains
✔️ Dieterle—Legionella
✔️ Gomori methenamine—Pneumocystis
✔️ fungi

⭕️ Acid fast (Ziehl-Neelsen or Kinyoun)
✔️ Mycobacterium
✔️ Nocardia (partially AF)
✔️ Cryptosporidium
✔️ Isospora
✔️ Cyclospora
✔️ Microsporidia (oocysts in feces)

⭕️ India ink
✔️ Cryptococcus (if negative not a reliable diagnostic method)

⭕️ Calcofluor white
✔️ fungi

⭕️ Giemsa
✔️ Plasmodium
✔️ Babesia
✔️ Trypanosoma
✔️ Leishmania
✔️ Histoplasma capsulatum in RES cells.



https://www.tg-me.com/general_laboratory_information
♨️ Urease Positive

✔️ All Proteus species produce urease; this leads to alkaline urine and may
be associated with renal calculi.
✔️ Ureaplasma (renal calculi)
✔️ Nocardia
✔️ Cryptococcus (the fungus)
✔️ Helicobacter.

⭕️ (mnemonic: PUNCH)

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Acquired aplastic anemia (AA) and paroxysmal nocturnal hemoglobinuria (PNH) are pathogenically related nonmalignant bone marrow failure disorders linked to T-cell–mediated autoimmunity; they are associated with an increased risk of secondary myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Approximately 15% to 20% of AA patients and 2% to 6% of PNH patients go on to develop secondary MDS/AML by 10 years of follow-up.
Factors determining an individual patient’s risk of malignant transformation remain poorly defined.
Recent studies identified nearly ubiquitous clonal hematopoiesis (CH) in AA patients.
Similarly, CH with additional, non-PIGA, somatic alterations occurs in the majority of patients with PNH.
Factors associated with progression to secondary MDS/AML include longer duration of disease, increased telomere attrition, presence of adverse prognostic mutations, and multiple mutations, particularly when occurring early in the disease course and at a high allelic burden.
Here, we will review the prevalence and characteristics of somatic alterations in AA and PNH and will explore their prognostic significance and mechanisms of clonal selection.
We will then discuss the available data on post-AA and post-PNH progression to secondary MDS/AML and provide practical guidance for approaching patients with PNH and AA who have CH.

https://ashpublications.org/blood/article/136/1/36/456026/Secondary-myelodysplastic-syndrome-and-leukemia-in
♨️ Catalase positive

✔️ All staphylococci
✔️ Pseudomonas aeruginosa
✔️ Candida
✔️ Aspergillus
✔️ Enterobacteriaceae.

⭕️ Catalase positive organisms are major problems in chronic granulomatous disease (CGD).

https://www.tg-me.com/general_laboratory_information
Lab abbreviation.pdf
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أكثر من 500 إختصار مخبري وكذلك بعض الإختصارات الطبية مرتبة أبجدياً.
♨️ Zeta Potential
Zeta potential is the difference in negative charge between the inner and outer surfaces of the cloud.

✔️ The cross-linking of cells is affected most by zeta potential.
When cells are suspended in isotonic saline, a cloud of negative ions surrounds the red cell.
The cloud of negative charge surrounding the cells causes them to repel one another.
The distance between the red cells is proportional to the zeta potential.
Reduction of zeta potential allows the red cells to approach one another and aids in lattice formation.
Zeta potential may be reduced by suspension of the cells in isotonic saline; addition of a potentiating substance such as:
albumin,
low ionic strength substance (LISS),
polyethylene glycol (PEG),

✔️ treatment of the cells with enzymes.
✔️ Additional forces that are involved in antigen-antibody reactions are summarized as followed

Ionic Bonding (Electrostatic Forces)
opposite charges on two molecules attracting each other
Hydrogen Bonding
attraction of two electronegative atoms to a positively charged hydrogen atom
Hydrophobic Bonding
bond between antigen and antibody that excludes a water molecule; usually a weak bond
Van der Waals Forces
attractive or repulsive forces between molecules or parts of molecules;
excludes covalent bonds or electrostatic forces.


https://www.tg-me.com/general_laboratory_information
Active cutaneous Leishmania at leg
This ulcer from a month ago and after months of infected by sand fly
♨️ ACTIVE IMMUNIZATION VERSUS
PASSIVE IMMUNIZATION

✔️ active immunization are antibodies stimulated by direct contact with the antigen,
Initial antigen exposure stimulates lymphocyte processing of the antigen and subsequent production of antibodies.

✔️ Passive antibodies are either administered via injection or cross the maternal placental barrier,
Antibodies may be obtained from an external source and serve a temporary protective role.


https://www.tg-me.com/general_laboratory_information
♨️ Antigens and Antibodies
in ABO Blood Groups.

https://www.tg-me.com/general_laboratory_information
♨️ A1 and A2 Subgroups

✔️ Group A antigens can be differentiated into multiple subgroups.
✔️ The two major subgroups are A1, 80% of Group A individuals, and A2, 20% of group A individuals.
Persons typing as AB can be divided into the same percentages of A antigen presentation.
A1B make up approximately 80% and A2B are 20% of all AB individuals.
✔️ A1 and A2 antigens have qualitative and quantitative differences.

⚫️ A1 and A2 red cells have differing amounts of antigens on the cell surface.
The A1 gene produces a transferase that has a greater ability to convert H antigen to A antigen than the A2 gene.
This quantitative difference results from the kinetics of the reaction catalyzed by each of the transferases.
There are also differences in the quantity of transferase produced.
Individuals exhibiting the A1 phenotype have five to ten times more transferase than those with an A2 phenotype.
Two mutations have been detected
that produce this A2 phenotype.
These are: a Pro-156Leu substitution and a single nucleotide deletion (nucleotide 1060).
These substitutions are responsible for the decreased enzyme activity that differentiates A2 from A1 cells.

⚫️ The antigens also differ qualitatively.
A2 antigens are composed mainly of linear oligosaccharide chains while
the A1 cells have a greater number of branched chains.
In routine testing, this qualitative difference is not detectable but can be determined biochemically.
Typing of A1 and A2 cells is unremarkable with routine antisera.
Both A1 and A2 cells will react equally with anti-A and anti-A,B.
The lectin, Dolichos biflorus, is used to obtain an extract with anti-A1 specificity.
Dolichos biflorus will react specifically with A1 cells and will be negative with A2 cells.
A2 individuals can develop antibodies to the A1 antigens.
The typical reaction pattern of reverse grouping in a group A individual is no agglutination with the A cells (no anti-A) and agglutination with B cells (anti-B present).
In A2 persons with an anti-A1, the A cells will also be agglutinated in the reverse grouping.
This discrepancy should be confirmed by testing the red cells with the Dolichos biflorus lectin.

https://www.tg-me.com/general_laboratory_information
♨️ ABO ANTIBODIES

✔️ Antibodies directed against ABO antigens are the most important antibodies in transfusion medicine.
This is a profound, but true statement.
The ABO blood group presents a unique situation in Immunohematology.
It is the only example of a blood group where each individual produces antibodies to antigens not present on the red cells.
These ABO antibodies were originally thought to be natural
antibodies formed with no apparent antigenic stimulus.
antibodies are not stimulated by exposure to red cells, they may also be considered non-red cell stimulated antibodies.
some form of an antigenic stimulus must exist.
The proposed mechanism is environmental. These “naturally occurring” substances resemble A and B antigens and stimulate the production of complementary antibodies to the antigens that
are not present on the red cell surface.

✔️ Newborns have no ABO antibodies.
newborns are tested, only a forward group is performed.
Newborns may exhibit passive ABO antibodies that have crossed the placental barrier.
Reverse grouping of a newborn or umbilical cord serum indicates
the blood group of the mother.

✔️ The child will begin antibody production, and have a detectable titer, at three to six months of age.
ABO antibody production
peaks at age five to ten years of age and continues in immunocompetent individuals throughout life.
Titers begin to wane in the elderly.

https://www.tg-me.com/general_laboratory_information
♨️ Sodium hypochlorite centrifugation technique to concentrate AFB .

1⃣ Transfer 1–2 ml of sputum to a
screw-cap container of 15–20 ml capacity.
2⃣ Add an equal volume of concentrated sodium hypochlorite (bleach) solution and mix well.
3⃣ Leave at room temperature for 10–15 minutes, shaking at intervals to break down the mucus in the sputum.
4⃣ Add about 8 ml of distilled water, Mix well.
5⃣ Centrifuge at 3000 g for 15 minutes.
6⃣ Using a Pasteur pipette, remove and discard the supernatant fluid ,Mix the sediment.
7⃣ Transfer a drop of the well-mixed sediment to a clean scratch-free glass slide ,Spread the sediment to make a thin preparation and allow to air-dry.
8⃣ Heat-fix the smear and stain it using the Ziehl Neelsen technique .

https://www.tg-me.com/general_laboratory_information
يَا مَنْ يَعِزّ عَلَيْنَا أنْ نُفَارِقَهُمْ
وَجدانُنا كُلَّ شيءٍ بَعدَكمْ عَدَمُ

- المتنبي


فلسطين قضية مركزية
إنَّ الصـلاةَ على النـبيِّ وســيلةٌ
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‏صلّوا عليهِ و سلّموا كي تغنَموا
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2025/07/06 20:36:17
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