Ecoli Dx: PCR Kits for Clinical Diagnostics and Human Genome Testing

Sexually transmitted disease (STD), also known as a sexually transmitted infection (STI) or venereal disease (VD), is an illness that has a significant risk of transmission between humans by means of human sexual behavior. While in the past these illnesses have mostly been referred to as STDs or VD, in recent years the term sexually transmitted infections (STIs) has been preferred, as it has a broader range of meaning; a person may be infected, and may potentially infect others, without having a disease.

Some STIs can also be transmitted via the use of IV drug needles after its use by an infected person, as well as through childbirth or breastfeeding. STI is a broader term than STD. Infection is a colonization by a parasitic species, which may not cause any adverse effects. In a disease the infection leads to impaired or abnormal function. In either case, the condition may not exhibit signs or symptoms. Increased understanding of infections like HPV, which infects most sexually active individuals, but cause disease in only a few has led to increased use of the term STI.

Many infectious diseases, including the common cold, influenza, pneumonia and most others that are transmitted person-to-person can also be transmitted during sexual contact if one person is infected. However, even though these diseases may be transmitted during sex, they are not considered STDs. MultiPlex Real-Time PCR technology allows using primers and probes for several (for up to 5) DNA targets in one tube. Amplification products identification runs for each DNA target on a different optical channel.

The sensitivity of these tests is not affected by changing the number of infections. Each mono- and multiplex PCR kit contains independent Internal Control (IC) for determination of DNA extraction efficiency and PCR process. Presence of the Internal Control signal/band shows, that the DNA extraction process and amplification steps were sufficient for significant results interpretation.

Human papillomaviruses (HPVs) are a group of more than 150 related viruses. They are called papillomaviruses because certain types may cause warts or papillomas, which are benign (noncancerous) tumors. Some HPVs, such as those that cause common warts that grow on hands and feet, do not spread easily. However, more than 40 HPV types are sexually transmitted and these HPVs spread very easily through genital contact.

Some types of sexually transmitted HPVs cause cervical cancer and other types of cancer. These are called high-risk, oncogenic, or carcinogenic HCR HPVs (about 13 types). Other sexually transmitted types of HPV do not appear to cause cancer and are called low-risk HPVs (LCR HPVs).

Although genital HPV infections are very common, most occur without any symptoms and go away without any treatment within a few years. However, some HPV infections can persist for many years. Persistent infections with high-risk HPV types can cause cell abnormalities. If untreated, areas of abnormal cells (lesions) can in some cases develop into cancer.

Some types of sexually transmitted low-risk HPVs cause warts to appear on or around the genitals or anus. Most genital warts are caused by two HPV types, HPV-6 and HPV-11. Warts may appear within several weeks after sexual contact with a person who is infected with HPV, or they may take months or years to appear, or they may never appear.

HIV stands for ‚human immunodeficiency virus‘. HIV is a virus (of the type called retrovirus) that infects cells of the human immune system (mainly CD4 positive T cells and macrophages), and destroys or impairs their function. Infection with this virus results in the progressive deterioration of the immune system. Within the retrovirus family, HIV belongs to a subgroup known as lentiviruses, or „slow“ viruses. Lentiviruses are known for having a long time period between initial infection and the beginning of serious symptoms. Similar versions of HIV infect other non-human species, such as feline immunodeficiency virus (FIV) in cats and simian immunodeficiency virus (SIV) in monkeys and other non-human primates. The immune system is considered deficient when it can no longer fulfill its role of fighting off infections and diseases.

Immunodeficient people are more susceptible to a wide range of infections, most of which are rare among people without immune deficiency. Infections associated with severe immunodeficiency are known as ‚opportunistic infections‘, because they take advantage of a weakened immune system. Some people at the time of seroconversion develop “Acute retroviral syndrome” which is a glandular fever-like illness with fever, rash, joint pains and enlarged lymph nodes. Seroconversion refers to the development of antibodies to HIV and usually takes place between 1 and 6 weeks after HIV infection has happened.

Whether HIV infection causes initial symptoms or not, an HIV infected person is highly infectious during this initial period and can transmit the virus to another person. The only way to determine whether HIV is present in a person's body is by testing for HIV antibodies, DNA or RNA. After HIV has caused progressive deterioration of the immune system, increased susceptibility to infections may lead to symptoms. Primary HIV infection - may be asymptomatic or experienced as Acute retroviral syndrome. Clinical stage 1 - asymptomatic or generalized swelling of the lymph nodes Clinical stage 2 - minor weight loss, mucocutaneous manifestations and recurrent upper respiratory tract infections Clinical stage 3 - includes unexplained chronic diarrhea, unexplained persistent fever, oral candidiasis or leukoplakia, severe bacterial infections, pulmonary tuberculosis, and acute necrotizing inflammation in the mouth. Some people with clinical stage 3 have AIDS. Clinical stage 4 - includes 22 opportunistic infections or cancers related to HIV. All people with clinical stage 4 have AIDS.

Respiratory tract infection refers to any of a number of infectious diseases involving the respiratory tract. An infection of this type is normally further classified as an upper respiratory tract infection (URI) or a lower respiratory tract infection (LRI). Lower respiratory infections, such as pneumonia, tend to be far more serious conditions than upper respiratory infections, such as the common cold. URIs represents the most common acute illness evaluated in the outpatient setting and is a nonspecific term used to describe acute infections involving the nose, paranasal sinuses, pharynx, larynx, trachea and bronchi. URIs range from the common cold - typically a mild, self-limited, catarrhal syndrome of the nasopharynx - to life-threatening illnesses such as epiglottitis. Symptoms of URIs can include cough, sore throat, runny nose, nasal congestion, headache, low-grade fever, facial pressure and sneezing. Influenza is a systemic illness that involves the upper respiratory tract and should be differentiated from other URIs. LRIs are generally more serious than URIs. LRIs are the leading cause of death among all infectious diseases. The two most common LRIs are bronchitis and pneumonia. Influenza affects both the upper and lower respiratory tracts, but more dangerous strains such as the highly pernicious H5N1 tends to bind to receptors deep in the lungs. Viruses cause most URIs, with rhinovirus, parainfluenza virus, coronavirus, adenovirus, respiratory syncytial virus, coxsackievirus and influenza virus. Human metapneumovirus is a newly discovered agent causing URIs. Group A beta-hemolytic streptococci (GABHS) cause 5% to 10% of cases of pharyngitis in adults. Other less common causes of bacterial pharyngitis include group C beta-hemolytic streptococci, Corynebacterium diphtheriae, Neisseria gonorrhoeae, Arcanobacterium haemolyticum, Chlamydia pneumoniae, Mycoplasma pneumoniae and Herpes simplex virus. Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis are the most common organisms that cause the bacterial superinfection of viral acute sinusitis. Less than 10% of cases of acute tracheobronchitis are caused by Bordetella pertussis, B. parapertussis, M. pneumoniae or C. pneumoniae.

The Herpesviridae are a large family of DNA viruses, that cause diseases in humans. The family name is derived from the Greek word herpein („to creep“), referring to the latent, recurring infections typical of this group of viruses. Herpesviruses all share a common structure - all herpes viruses are composed of relatively large ds linear DNA encoding 100-200 genes and all herpes viruses are nuclear-replicating - the viral DNA is transcibed to RNA within the infected cell's nucleus. Infection is initiated when a viral particle contacts a cell. Following binding, the virion is internalized and dismantled, allowing viral DNA to migrate to the cell nucleus, where replication of viral DNA and transcription of viral genes occurs. During symptomatic infection, infected cells transcribe lytic viral genes. In some host cells, a small number of viral genes termed latency-associated transcript (LAT) accumulate instead. In this fashion, the virus can persist in the cell (and thus the host) indefinitely. While the primary infection is often accompanied by a self-limited period of clinical illness, long-term latency is symptom-free. Reactivation of latent viruses has been implicated in a number of diseases. Following activation, transcription from latency-associated LAT to multiple lytic genes lead to enhanced replication and virus production. Clinically, lytic activation is often accompanied by the emergence of non-specific symptoms such as low-grade fever, headache, sore throat, malaise and rash as well as clinical signs such as swollen or tender lymph nodes and immunological findings such as reduced levels of natural killer cells. In this family, there are eight human herpes-viruses: Herpes Simplex virus type 1 and 2, VZV, CMV, EBV and HHV-6, HHV-7, HHV-8.

TORCH complex (also known as STORCH, TORCHES or the TORCH infections) is a medical acronym for a set of perinatal infections (i.e. infections that are passed from a pregnant woman to her fetus). The TORCH infections can lead to severe fetal anomalies or even fetal loss. They are a group of viral, bacterial, and protozoan infections that gain access to the fetal bloodstream transplacentally via the chronic villi. Hematogenous transmission may occur at any time during gestation or occasionally at the time of delivery via maternal-to-fetal transfusion.

The TORCH complex was originally considered to consist of four conditions, with the „TO“ referring to „Toxoplasma“. The four-term form is still used in many modern references, and the capitalization „TORCH“ is sometimes used in these contexts. Alternatively, the „O“ is redefined as „other“, and the acronym is spelled out as follows:

1. T – Toxoplasmosis/Toxoplasma gondii
2. O – Other infections (see below)
3. R – Rubella
4. C – Cytomegalovirus
5. H – Herpes simplex virus

The „other agents“ included under O are Hepatitis B, Coxackievirus, Syphilis, Varicella-Zoster virus, HIV and Parvovirus B19.

Purulent infections are characterized by purulent inflammation of tissues that arise in the implementation of pyogenic bacteria, most commonly Streptococcus, Staphylococcus, more rarely Pseudomonas or E. coli. For some common infections local centers of suppuration (glanders, bubonic plague, cutaneous anthrax) are typical. Purulent infection can develop in the form of the disease (furuncle, carbuncle, erysipelas, osteomyelitis, etc.), or as a complication of the wound. In some cases, purulent focus can disappear spontaneously or may be disposed of after a simple intervention, in others requires a complex operation. Generalization of the purulent process may lead to the development of general purulent infection, i.e., sepsis. Purulent infections are very often resistant to antibiotics.

• Vibrio cholerae
• Bacillus anthracis
• Brucella species
• Dengue fever virus
• Leptospira species
• Borrelia burgdorferi sensu lato
• Tick-borne encephalitis virus
• West Nile fever virus
• Crimean-Congo hemorrhagic fever virus
• Yersinia pestis
• Coxiella burnetii
• Ebola Zaire virus
• Zika virus
• Yellow fever virus
• Rickettsia

Leucosis Quantum M-bcr

Chronic myelogenous (or myeloid) leukemia (CML), also known as chronic granulocytic leukemia (CGL), is a cancer of the white blood cells. It is a form of leukemia characterized by the increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood. CML is a clonal bone marrow stem cell disorder in which proliferation of mature granulocytes (neutrophils, eosinophils, and basophils) and their precursors are the main finding. It is a type of myeloproliferative disease associated with a characteristic chromosomal translocation called the Philadelphia chromosome. CML is now largely treated with tyrosine kinase inhibitors (TKIs), such as imatinib, dasatinib or nilotinib, which has led to dramatically improved survival rates since their introduction in the last decade.

CML was the first malignancy to be linked to a clear genetic abnormality, the chromosomal translocation known as the Philadelphia chromosome. In this translocation, parts of two chromosomes (the 9th and 22nd by conventional karyotypic numbering) switch places. As a result, part of the BCR („breakpoint cluster region“) gene from chromosome 22 is fused with the ABL gene on chromosome 9. This abnormal „fusion“ gene generates a protein of p210 or sometimes p185 weight (p210 is short for 210 kDa protein, a shorthand used for characterizing proteins based solely on size). Because abl carries a domain that can add phosphate groups to tyrosine residues (a tyrosine kinase), the bcr-abl fusion gene product is also a tyrosine kinase.

The fused BCR-ABL protein interacts with the interleukin 3 beta (c) receptor subunit. The bcr-abl transcript is continuously active and does not require activation by other cellular messaging proteins. In turn, BCR-ABL activates a cascade of proteins that control the cell cycle, speeding up cell division. Moreover, the BCR-ABL protein inhibits DNA repair, causing genomic instability and making the cell more susceptible to developing further genetic abnormalities. The action of the BCR-ABL protein is the pathophysiologic cause of chronic myelogenous leukemia.

With improved understanding of the nature of the BCR-ABL protein and its action as a tyrosine kinase, targeted therapies (the first of them was imatinib mesylate) that specifically inhibit the activity of the BCR-ABL protein, have been developed. These tyrosine kinase inhibitors can induce complete remissions in CML, confirming the central importance of bcr-abl as the cause of CML.

Clinically, leukemia is manifested in three distinct phases: chronic, accelerated, and blast. Most patients present in the chronic phase, a stage that is typically indolent in nature. Mature granulocytes are found, but patients typically have an increase in the number of myeloid progenitor cells found in the blood. Left untreated, the disease progresses to an accelerated phase followed by blast crisis, which is inevitably fatal. During blast phase, hematopoietic differentiation is blocked and blast cells accumulate in the bone marrow and peripheral blood. Expression of BCR-ABL onco-proteins in hematopoietic cells induces resistance to apoptosis, growth factor independence and leukemogenesis.

• Nucleic Acid Extraction Kits
• Reverse Transcription
• Transport and Storage Media