BACTERIOLOGY

 

BACTERIOLOGY

MEDICAL MICROBIOLOGY

 

MEDICAL MICROBIOLOGY:  Microbiology is a broad specialty that covers a wide range of topics and can be taken as both a basic science and a medical science.  In our discussions here, we are are going to focus on the medical part of the course and we shall be looking at the microbes that causes diseases in humans.  The course basically cover the study of bacteria also known as bacteriology, the study of viruses also known as virology, the study of fungi also known as Mycology,

RELATED;

1.  BACTERIOLOGY

2.  MEDICAL VIROLOGY

3.  MEDICAL MYCOLOGY

NORMAL FLORA AND THE HUMAN BODY

 

INTESTINAL TRACT: At birth the intestine is sterile. In breast-fed children the intestine contains large number of lactic acid streptococci and lactobacilli. In bottle-fed children a mixed flora exists in the bowel and lactobacilli are less prominent. Diet has a marked influence on the composition of intestinal and faecal flora. Bowels of newborns in intensive care nurseries tend to be colonized with pathogenic organisms such as Klebsiella, Citrobacter and Enterobacter.

OESOPHAGUS AND THE STOMACH: In oesophagus and stomach the number of organisms is that swallowed with the food and it is temporary because the acidity of the stomach is protective. In conditions where there is decreased acidity of the stomach there are chances of increased number of organisms present in the stomach.

IN THE INTESTINES: The number of bacteria increases progressively beyond the duodenum to the colon, being comparatively low in the small intestine. In the upper intestine, lactobacilli and enterococci predominate, but in the lower ileum and caecum the flora is faecal. In normal adult colon the resident flora is predominantly anaerobic ranging between 96-99% consisting of Bacteroides, Fusobacterium, Anaerobic lactobacilli, Clostridium sp. and anaerobic streptococci.

Only about 4% are facultative aerobes consisting of gram-negative coliform bacteria, Enterococci, Lactobacilli, Proteus, Pseudomonas, Candida and others. More than 100 distinct types of organisms occur regularly in normal faecal flora. Prevalence of drug resistant organisms in the intestine serves as a source of plasmid-mediated drug resistance in the bacteria. Antimicrobial drug resistance

IN THE URETHRA: The anterior urethra of both sexes contains small numbers of the same types of organisms found on the skin and perineum. The organisms regularly appear in the normal voided urine. The commonly encountered organisms are Coagulase negative Staphylococci, Enterococci, Non-pathogenic neisseriae, Non-pathogenic mycobacteria, Various enteric gram-negative rods, Corynebacterium. In addition to the mentioned above, there is occasionary; Trichomonas vaginalis, Candida albicans, Staphylococcus aureus.

IN THE VAGINA: The usual microflora of the vagina from the menarche to the menopause is dominated by lactobacilli designated as Doderlien’s bacilli. The nature of the flora in the vagina depends on the pH of its secretions and it enzyme content. At birth the vagina is sterile. In the first 24 hours it is invaded by micrococci, enterococci and diphtheroids. With the appearance of glycogen the pH changes to acidic and the nature of the flora changes. The organisms normally encountered in the vagina are; Anaerobic streptococci, Beta haemolytic streptococci, Bacteroides, Gardnerella vaginalis, Ureaplasma urealyticum, Listeria monocytogenes, Staphylococcus aureus. Vaginal organisms present at the time of delivery may infect the newborn.

MOUTH AND UPPER RESPIRATORY TRACT: The flora of the nose consists of prominent corynebacteria, staphylococci (Staph. epidermidis and Staph. aureus) and streptococci. The mucous membrane of the mouth and pharynx are often sterile at birth but may be contaminated by passage through the birth canal. Within 4-12 hours after birth, viridans streptococci become established as the most prominent members of resident flora and remain so for life. Early in life, aerobic and anaerobic staphylococci, gram-negative diplococci, diphtheroids and occasional lactobacilli are added. When teeth begin to erupt anaerobic spirochaetes establish themselves along with anaerobic vibrios and lactobacilli. Actinomyces spp. are normally present in tonsillar tissue and various protozoa may also be present. Candida spp. can also be present in mouth. In the pharynx and trachea, a similar flora establishes itself. A few bacteria are found in normal bronchi. Small bronchi and alveoli are normally sterile. The predominant organisms in the upper respiratory tract, particularly the pharynx are non-haemolytic and alpha haemolytic streptococci and neisseriae.

RELATED;

1.  Enterobacteriaceae

2.  Streptococcus

3.  Bacteriology

REFERENCES

THE HUMAN MICROBIOME

 

INTRODUCTION:  Until recently, our view of human microbiology was shaped by what microorganisms were isolated from persons with acute infection. However, over time it has become apparent that the diversity of microorganisms observed from microscopy or genetic sequencing was far greater than the microorganisms that were isolated from traditional culture techniques. The human body harbors numerous species of bacteria, viruses, fungi, and protozoa, referred to as the human microbiota or microbiome.

RELATIONSHIP OF THE MICROBIOME AND THE HUMAN BODY:  The great majority of these are commensals, defined as organisms that live symbiotically on or within the human host but rarely cause disease. Anatomic sites where bacteria are normally found include the skin (staphylococci and diphtheroids), oropharynx (streptococci, anaerobes), large intestine (enterococci, enteric bacilli), and vagina (lactobacilli).  Enteric bacilli

DISEASES ASSOCIATED WITH THE MICROBIOME:  Microbes do not exist in the human body in isolation but in complex communities and habitats. Imbalances in the composition of these habitats are associated with human infection and disease. One example of an infection that can result from a perturbed microbiota community is that caused by Clostridium difficile. C. difficile is an anaerobic gram-negative rod that causes intestinal disease in the setting of antibiotic administration. Antibiotics alter the structure and function of an individual’s gut microbiota, reducing the body’s innate resistance to colonization with C. difficile organisms (and other enteric pathogens) and providing them a niche to multiply and elaborate their enterotoxins. Innate immunity

ANTIBIOTIC INTERACTION AND THE MICROBIOME:  Similarly, broad-spectrum antibiotics will destroy normal vaginal flora, such as lactobacilli, and allow overgrowth of Candida (yeast) species, resulting in Candida vaginitis.  Determining when an isolate is a component of the normal flora rather than an invasive pathogen may be difficult. For example, culture of staphylococci from a blood sample may represent skin contamination at the time of phlebotomy or may indicate a potentially life-threatening bloodstream infection. Helpful clues include burden of organism (eg, number of positive blood cultures), symptoms and signs of infection (eg, cough, fever), and the presence of inflammatory cells (eg, polymorphonuclear cells in the sputum and an increased proportion of immature neutrophils in the blood).  

Isolation of an obligate pathogen such as Mycobacterium tuberculosis from any anatomic site is diagnostic of infection. Fortunately, few microorganisms are absolute pathogens. For example, Neisseria meningitidis, a major bacterial cause of meningitis, can be cultured from the oropharynx of as many as 10% of asymptomatic individuals, in which case it represents transient normal flora. Even if asymptomatic, the host can serve as a carrier, transferring bacteria to susceptible individuals. Infections resulting from commensals that rarely cause disease (eg, Candida albicans) or organisms ubiquitous in the environment that are generally not considered human pathogens (eg, Aspergillus) are termed opportunistic infections. These infections occur almost exclusively in immunocompromised hosts, such as HIV-infected patients or transplant recipients.  HIV/AIDS 

The agents are opportunists in that they take advantage of impaired host immunity to cause infection but rarely cause disease in a healthy host. The presence of bacteria on a body surface without causing disease is called colonization, whereas invasion of the tissues by a microorganism that causes disease is termed infection. The site from which an organism is cultured is important in differentiating colonization from infection. Growth of any microorganism from a normally sterile site such as blood, cerebrospinal fluid,individuals are then at increased risk for life-threatening infections such as Pseudomonas pneumonia.

RELATED;

1.  Bacteriology

2.  Virology

3.  Normal flora of the human body

4.  Dynamics of infectious diseases

REFERENCES

TREPONEMA PALLIDUM

 

INTRODUCTION: T. pallidum is the causative agent of venereal syphilis in man. Typical organisms are slender spirals measuring about 0.2 μm in width especially in wet preparations, and 6-15 μm in length. The spiral coils are regularly spaced at a distance of 1 mm from one another. In dry preparations the width is about 0.13 μm. The two ends of the spirochaete are tapering. It is actively motile, exhibiting rotation round the long axis, backward and forward movements and flexion of the whole body.  During motion the primary spirals are maintained though secondary curves appear and disappear in succession. When dark field microscopy is not available, the organism can be detected in wet films of the exudate mixed with India ink.

STAINING: T. pallidum cannot be stained by simple aniline dyes or by Gram’s method. In films stained with Giemsa’s prolonged method for 24 hours the organisms appear as delicate pink threads. It can be stained by silver impregnation methods. Fontana’s method is useful for smears and Levaditi’s for tissue sections.

MULTIPLICATION: The spirochaetes multiply by transverse binary fission. Divided organisms may adhere to one another for sometime. The division time is 30 hours, while the division time of cultivable Reiter’s strain is about 10 hours. Treponema pallidum, carateum and pertenue have not been cultivated in artificial media, not even in chick embryo or tissue culture where they appear only to persist for a long time. In proper suspending fluids and in the presence of reducing substances, T. pallidum may remain motile for 3-6 days at 25⁰C. In whole blood or plasma stored at 4⁰C, organisms remain viable for atleast 24 hours, which is important in blood transfusion services.

RESISTANCE: Drying kills the spirochaetes rapidly as does the elevation of the temperature to 42⁰C for about 60 minutes. When stored at referigerator temperatures, the organism is killed in 1-3 days. Stored frozen at –70⁰C in 10 percent glycerol or in liquid nitrogen the organism remains viable for 10-15 years. Resistance to penicillin has not been demonstrated in syphilis.

RELATED;

1.  PENICILLIN 

2.  ANTIMICROBIAL DRUG RESISTANCE 

3.  GRAM NEGATIVE BACTERIA

REFERENCES

VIRIDANS STREPTOCOCCI

INTRODUCTION: This is a heterogenous group of very poorly defined alpha haemolytic streptococci that are present in abundance in the mouth and pharynx. About 50% of bacterial endocarditis is caused by these bacteria. Since they do not have a defined group carbohydrate antigen, no correlation exists between serologic and physiologic characteristics of these strains.  The viridans streptococci comprise of six species viz. Strep. pneumoniae, Strept. mutans, Strept. sanguis, Strept. salivarius, Strept. milleri and Strept. mitior.

CLINICAL SIGNIFICANCE: When isolated from mouth, throat or respiratory tract, viridans streptococci are generally regarded as harmless commensals. The medical importance of this group is because of its association with dental caries, sepsis and bacterial endocarditis. S. milleri is associated with deep sepsis, including liver and brain abscesses. S. mutans, S. mitior and S. sanguis are involved in the production of dental caries. Endocarditis can be caused by S. mitior and S. sanguis. Nothing much is known about the pathogenicity of S. salivarius but is believed to be capable of causing dental caries.  Streptococcus MG group is one of the viridans group which share certain antigens with Mycoplasma pneumoniae

Dental Caries: It is a multifactorial disease that results only when all dependent factors coincide. Three important factors that cause it are:

1. Susceptibility of host and teeth. Pits, fissures and spaces tend to entrap food and let microflora flourish.

2. Excessive dietary sucrose intake which can be fermented by bacteria to produce acid which can demineralize the dental enamel.

3. Cariogenic microflora which comprises of various species of streptococci and lactobacilli. Among the streptococci, S. mutans, S. mitior and S. sanguis have been shown to cause dental caries even in experimental animals. Species of Lactobacillus which are generally present in oral cavity and have been incriminated as possible causative agents of dental caries are L. casei, L. fermentum, Bifidobacterium bifidum and L. acidophilus.

Infective Endocarditis: Viridans streptococci account for about 40% of the cases of infective endocarditis. Strep. sanguis and Strep. mitis are most commonly incriminated followed by Strep. mutans and Strep. milleri.

Factors predisposing to infective endocarditis include:  i. Cardiac factors; Rheumatic heart disease, Congenital heart disease, Cardiac surgery, Prosthetic heart valves.  ii. Non-cardiac factors; Dental manipulations, Sepsis.

RELATED;

1.  STREPTOCOCCI

2.  STAPHYLOCOCCI

3.  BACTERIOLOGY

REFERENCES

HOW TO BREAK THE CHAINS OF INFECTIOUS AGENTS

HOW TO BREAK THE CHAINS OF INFECTIOUS AGENTS:  Day to day we meet microbes and infectious agents from the air we breath, the food we eat, the water we drink and the equipment we use.  Our fear of encountering microbes is limited, but because of two basic reasons; 1) We tend to know much less about their level of infectiousness.  2)  The are just very tiny for us to observe with a naked eye.  The overall goal of humans to be safe and free from the diseases caused by microbes, is to develop immunity against them and be able to prevent close contact with such microbes.  In our discussion here, we are going to look at some of the ways we can be free from some of the most common infectious agents.  But before we continue if you have not been following us, it requires you to read about the ways we get exposed to disease causing microbes from the link below; Dynamics of infectious diseases.

Cont..............................

RELATED;

1.  DYNAMICS OF INFECTIOUS DISEASES

RETROVIRUSES

 

INTRODUCTION:  Retroviruses are unique in the sense that the flow of genetic information is reverse to the universal flow.  In all other organisms, DNA is the store house of genetic information and from here it is transmitted to RNA.  In retroviruses the sequence is RNA to DNA and consequent use of the enzyme reverse transcriptase.  Genetic information is passed on from RNA to DNA through RNA-dependent DNA polymerase (reverse transcriptase).

INVASIVENESS OF RETROVIRUSES:  The viral genetic information in DNA form is called as provirus.  This is capable of integration into the host genome.  On activation of provirus, virus specific proteins are manufactured. 

CLASSIFICATION:  The family Retroviridae comprised of three subfamilies: Oncovirinae, Lentivirinae and Spumavirinae.

HUMAN T CELL LEUKAEMIA VIRUSES:  The virion of human T cell leukaemia virus (HTLV) comprises icosahedral core containing the RNA genome and surrounded by an envelope acquired as the virion buds through the host cell membrane.  Virus specific envelope glycoproteins are inserted within the membrane that surrounds the virus.

Antigens:  Three structural antigens are recognised in HTLV.  These are core antigen, envelope antigen and RT antigen. The RT or in full Reverse Transcriptase antigen is derived from a polypeptide precursor which on being cleaved results into RT, protease and endonuclease.  RT is quite antigenic and sera from infected patients contain antibody to it.

HUMAN IMMUNODEFICIENCY VIRUS:  Emergence of this deadly disease appeared when the first few cases of AIDS were detected in June, 1981 by the US. Centers for Diseases Control and Prevention (CDC).  They reported a cluster of Pneumocystis pneumonia (PCP) caused by a form of Pneumocystis carinii, now recognised as a distinct species Pneumocystis jiroveci, in five homosexual men in Los Angeles.  The disease was originally dubbed GRID, or Gay-Related Immune Deficiency, but health authorities soon realized that nearly half of the people identified with the syndrome were not homosexual men.  In 1981, the CDC introduced the term AIDS to describe the newly recognised syndrome, though it was still casually referred to as GRID.  In 1983, scientists led by Luc Montaginer at the Pasteur Institute in France first discovered the virus that causes AIDS.  They called it lymphadenopathy associated virus (LAV).  A year later a team led by Robert Gallo of the United States confirmed the discovery of the virus, but they renamed it human T lymphotropic virus type III (HTLV-III).  The dual discovery led to considerable scientific disagreement, and it was not until President Mitterrand of France and President Reagan of the USA met that the major issues were resolved.  In 1986, both the French and the US names for the virus itself were dropped in favour of the new term, human immunodeficiency virus (HIV).

Global Scenario HIV infection in humans is now pandemic.  As of January 2006, the Joint United Nations Programmes on HIV/AIDS (UNAIDS) and the World Health Organization (WHO) estimate that AIDS has killed more than 25 million people since it was first recognized on December 1, 1981, making it one of the most destructive pandemics in recorded history.  In 2005 alone, AIDS claimed an estimated 2.4-3.3 million lives, of which more than 570,000 were children.  It is estimated that about 0.6% of the world’s living population is infected with HIV.  A third of these deaths are occurring in sub-Saharan Africa, retarding economic growth and increasing poverty.

Structure and Genome:   HIV is different in structure from other retroviruses.  It is about 120 nm in diameter which is around 60 times smaller than a red blood cell and roughly spherical.  It is composed of two copies of positive single stranded RNA that codes for the virus’s nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein P24.

RELATED;

1.  HIV/AIDS

2.  VIROLOGY

REFERENCES

FILOVIRUSES (MARBURG AND EBOLA VIRUSES)

INTRODUCTION: These are two related African viruses are subsumed under the name filoviruses, Marburg and Ebola. These pathogens cause hemorrhagic fevers with high lethality rates. The few described Marburg virus outbreaks apparently involve monkey populations. Ebola outbreaks are apparently becoming more frequent. The natural reservoir of the filoviruses is unknown.

DIAGNOSIS: By antigen assay, EM, and isolation.

PATHOGEN: The Marburg virus was isolated for the first time in 1967 as a result of three simultaneous outbreaks among laboratory staff in Marburg, Frankfurt, and Belgrade. The infection victims had been processing the organs of Cercopithecus (African green monkeys) from Uganda.

MORPHOLOGY AND STRUCTURE: Both the Marburg and Ebola viruses are threadlike, 14 µm-long viral particles, in some cases branched and 80 nm thick in diameter. Their surface consists of an envelope of host-cell membrane with viral spikes. The genome consists of antisense strand RNA in a helical nucleocapsid 50 nm in diameter.

PATHOGENESIS AND CLINICAL PICTURE: The Marburg and Ebola viruses cause socalled hemorrhagic fevers. The clinical picture first manifests with fever, headache, and neck pain, conjunctivitis and diarrhea, followed by hepatic, renal, and CNS involvement and finally, as a result of consumption coagulopathy, leads to extensive hemorrhaging and terminal shock. In terms of the anatomical pathology, nearly all organs show hemorrhages and fibrin deposits.

DIAGNOSIS: Only designated laboratories with special safety facilities can undertake isolation work on these viruses. Detection is either in blood with an electron microscope or using immunofluorescence on tissue specimens. The pathogens can be grown in cell cultures. Serodiagnosis is also possible.

EPIDEMIOLOGY AND PREVENTION: The reservoir of the Marburg and Ebola viruses is unknown. Subsequent to the Marburg outbreak in 1967 among lab personnel in Europe, Marburg viruses have only been found in Africa. The Ebola virus, named after a river in Zaire, has caused several outbreaks in Africa since 1976 in which lethality rates of 50–90% were observed. Imported Ebola infections have also been seen in monkey colonies in the USA and Italy. Protective suits and vacuum-protected plastic tents are no longer recommended for healthcare workers in contact with Marburg and Ebola patients (as with Lassa fever), since interhuman transmission is by excretions (smear infection) and in blood, but not aerogenic. Despite this fact, the high level of infectivity of any aerosols from patient material must be kept in mind during laboratory work and autopsies.

RELATED;

1. MICROBIAL INFECTIOUS CYCLES

2. INTRODUCTION TO VIROLOGY

3. VIRULENCE FACTORS OF MICROBES

4. VIRAL HEMORRHAGIC FEVERS

REFERENCES

MUMPS

INTRODUCTION: Mumps is predominantly, but not exclusively, a disease of childhood. Attacks in adult life are probably much more frequent than of measles, chickenpox and other common infections. No age is immune and there is no difference in the incidence between the two sexes although the disease appears to be more frequent in young male adults than in females. This difference is perhaps more apparent than real and due mainly to high incidence of orchitis which draws attention to what might otherwise be a short and soon-forgotten illness. Like measles mumps virus is a member of the family Paramyxoviridae.

PATHOGENESIS: Mumps is a typical systemic viral infection. The portal of entry of the virus is thought to be the upper respiratory tract. The time interval after exposure to virus before the appearance of the clinical features ranges from 14 to 21 days, with the usual incubation period being 16-18 days. After entering the host, the virus replicates and viraemia results. It leads to secondary invasion of several organs. Tissues such as the salivary glands (predominantly the parotids), meninges, testes, pancreas, ovaries, thyroid and heart may show evidence of infection. Virus is also excreted in urine and transient abnormalities in renal functions have been found.

Pathogenesis of damage to nervous system is poorly understood but may be due to direct lysis of cells and immunopathological mechanisms. All classes of specific immunoglobulins are induced by primary infection due to mumps virus. The IgM response persists for a few days but the IgG response is life-long. [Readabout immunoglobulins]

CLINICAL FEATURES: Mumps is a common contagious disease of children and young adults. It is characterised by the inflammation of salivary glands. Bilateral involvement of parotid glands is the commonest occurrence. Unilateral involvement of this gland can also occur. Similarly inflammation and swelling of submaxillary glands as well as sublinguals can also get infected. The disease is considered more notorious because of its complications of which orchitis and sterility in adult males is important. Infection with mumps virus during the first trimester of pregnancy may result into abortion. Though no teratogenicity has been demonstrated because of this virus, ample evidence for transplacental transmission is available.

LABORATORY DIAGNOSIS: In the presence of typical clinical picture the diagnosis of mumps is very simple and does not require any support from the laboratory. However, diagnosis by the virus isolation or serological techniques is most useful when the patient presents with an atypical or asymptomatic infection.

Clinical Specimens: Virus isolation from the spinal fluid, blood, saliva and urine confirms the diagnosis of recent mumps infection.

Isolation of the Virus Primary monkey kidney cell cultures are the most sensitive substrates for the isolation of this virus. These cells may be of rhesus or cynomolgus monkey origin. Continuous human cell lines such as HeLa and primary cell cultures of human amnion or human embryonic kidney can also be used for the growth of the virus. The virus produces a characteristic cytopathic effect (CPE) with large syncytia. Some strains may not produce CPE and their adsorption with guinea pig erythrocytes should be attempted to identify them. Rapid identification of mumps isolates can be achieved by immunofluorescence staining.

Serodiagnosis: Serological diagnosis of mumps infection can be very important, especially in those cases of meningitis or encephalitis that occur in the absence of parotitis. Serological methods for the diagnosis of mumps infection include complement fixation, haemagglutination inhibition, neutralisation, and ELISA. Use of ELISA to detect IgM is particularly suitable for early diagnosis of mumps infection with one serum specimen.

Treatment and Prevention: A live attenuated vaccine prepared from Jeryl Lynn strain of mumps virus was licensed for human use in the USA in 1967 and since then more than 100 million doses have been administered to children. Till recent past vaccines were prepared from following strains of mumps virus: Jeryl Lynn strain, Urabe strain, Rubini strain However, a higher incidence of vaccine associated meningitis because of the vaccine prepared from Urabe strain has forced the authorities in United Kingdom and Europe to discontinue the use of mumps vaccine prepared from this strain. The other two strains have not exhibited this kind of adverse reactivity. Mumps vaccine can be given along with or in combination with antigens of measles and rubella in combined form of measles-mumps-rubella (MMR). There is no specific treatment.

RELATED;

1. INTRODUCTION TO VIROLOGY  

2. HEMORRHAGIC FEVER VIRUSES  

3. VIRAL HEPATITIS

4.  MEDICAL MICROBIOLOGY

REFERENCES

HEMORRHAGIC FEVER VIRUSES

 

INTRODUCTION:  Bundibugyo ebolavirus belongs to genus Ebola virus which has other four species including; Zaire Ebolavirus( ZEBOV / EBOV); Taï Forest ebolavirus (formerly Côte d'Ivoire ebolavirus, CIEBOV / TAFV,) and Reston ebolavirus (REBOV / RESTV), Sudan ebola virus (SUDV / SEBOV).  Bundibugyo ebolavirus (BEBOV / BDBV)is one of the four ebolavirus that cause Ebola virus disease in human. It was first described in 2008 in Bundibugyo District. During 2007-2008, Bundibugyo ebola virus totally infected 116 human and 39 deaths. The mortality rate was 34%, which is lower than Zaire ebolavirus and Sudan ebolavirus.  

Bundibugyo ebolavirus (BDBV) made its first appearance on August 1 of 2007, when a viral hemorrhagic fever outbreak began in the Bundibugyo and Kikyo townships of Bundibugyo District in western Uganda. Blood samples from suspect cases were sent to the US Centers for Disease Control and Prevention, where the presence of an ebolavirus was confirmed on November 29, 2007. In depth analysis revealed that the present ebolavirus was a relative, but not identical, to the other four ebolaviruses known at the time. The outbreak was declared over on February 20, 2008.  A second outbreak was reported by the WHO August 17, 2012 suspected to have infected 15 and killed 10 including 3 health care workers in Isiro, Pawa and Dungu, Province Orientale, DRC.  2 of the cases have been confirmed to be Bundibugyo ebolavirus (BDBV). It is reported that bushmeat was the source. By Sept 3, the WHO reported that the number of cases had risen to 28, with 8 confirmed, 6 probable and 14 suspected, including 14 deaths, and as of 12 September, it had spread to Viadana and a total of 41 cases (9 laboratory confirmed, and 32 probable) have been reported from Haut-Uélé district in Province Orientale. Of these cases, 18 have been fatal. (5 confirmed and 13 probable). 18 healthcare workers are included among the probable cases. 28 suspected cases have also been reported and are being investigated. In a press release, the Democratic Republic of Congo announced a final tally of 77 cases (36 confirmed, 17 probable and 24 suspects) with 36 deaths.

[Source:  CDC factsheet]

RELATED;

1.  Virology

2.  The viral replication cycle

3.  Invasion of human CD4 cells by HIV virus

4.  REFERENCES

BODY'S LINES OF DEFENCE

BODY'S LINES OF DEFENCE:  When we talk about immunity in the human body, we are meaning the ability to fight emerging infections, and it is a necessity for every one to be alive.  The human body is a complex system that comes in contact with microbes on a daily basis some of which are the deadliest ever known such as; The hemorrhagic fever viruses, Tuberculosis, Hepatitis and HIV.  To spot a few examples like human contacts with fellows, fomites and the rest of the environment is to say nothing but the truth is that, the human body it's self is a home to millions of infectious agents some of which we end up calling normal flora or in other words, the human microbiome.  You can click here to continue reading about the normal flora.  In that respect, it is very easy for microbes to be introduced in the body via the skin, the oral cavity or through the respiratory system.

Our safety when it comes to microbes lies behind the ability of our bodies to recognize and destroy if possible any emerging microbes and or, develop immunity against such foreign bodies.  But it isn't that easy because everyday, there comes new and totally new antigens never met by our immune surveillance.  Yet even without that, the process of mutation and evolution keeps several known microbes change their rate of infectiousness via alterations of there genomes, again leaving the human body still prone to millions of infectious agents.  In our discussion here, we are going to look at the layers of defense as they are naturally gifted to the human body.

THE FIRST LINE OF DEFENCE:  The body's first line of defense are the barriers that covers the whole of it.  These include skin, one of the largest organ and system in the body and then the mucous membranes that are in the body openings.  Mucous membranes are present in the mouth, in the eyes, and around the anal and virginal canals.  The skin and it's integrity helps shielding the body from invaders and as long as it is intact, no microbe will be able to penetrate it except with use of penetrating sharp instruments.  This is one reason disinfectants are rubbed on any area where a venipuncture is going to be made.

On the other hand, mucous membranes are equipped with secretory immunoglobulins that are able to fight invading microbes.  You can click here to read more about Immunoglobulins.

THE SECOND LINE:  The body's second line of defense is inflammation.  The inflammatory process in the body aims at recruitment of immune cells that can fight infection at the sight of inoculation.  Where there is inflammation, the rapid and continuous inflow of blood comes with big numbers of white blood cells with an aim of eliminating if possible, the infectious agent.  I have discussed about inflammation in the previous articles and if you want to read about it, click here.

CONT..........

RELATED;

1.  NORMAL FLORA OF THE HUMAN BODY

2.  SPECIFIC IMMUNITY

3.  IMMUNOGLOBULINS

4.  BODY ORGANS

5.  THE INFLAMMATORY PROCESS

6.  HEMORRHAGIC FEVER VIRUSES

7.  VIRAL HEPATITIS

8.  THE HUMAN MICROBIOME

AUTOIMMUNITY

INTRODUCTION: The purpose of the immunological response is to protect the host and to discriminate between what is self and what is non-self for the host. The primary means by which the immune system recognises foreign antigens is through comparison with self major histocompatibility complex (MHC) determinants. Therefore, MHC serves as a yardstick against which foreign determinants can be measured. This implies that a mechanism exists in the host which can recognise its own self-antigens. At the same time mounting an immune response against self-antigens shall be devastating.

ORIGIN OF AUTOIMMUNITY: Recognition of self-determinants is normal and occurs during the generation of nearly all immune responses, whereas immunologic reactivity against self determinants can lead to autoimmune disease. The emergence of autoimmune disease is postulated to be due to mutation of a non-self reactive lymphocyte into self-reactive one, the activation of previous tolerant helper T cell or the inhibition of suppressor T cells.

CRITERIA FOR AUTOIMMUNE DISEASE: The disease must fulfil following criteria before it can be called as autoimmune disease.

a) The autoimmune response must be regularly associated with the disease.

b) A replica of the disease must be inducible in laboratory animals.

c) Immunopathologic changes in the natural and experimental diseases should parallel each other.

d) Transfer of autoimmune illness should be possible by the transfer of serum or lymphoid cells from the diseased individual to a normal recipient.

RELATIONSHIP OF HLA TYPES AND AUTOIMMUNE DISEASES: On the basis of various studies in animals, it has been shown that a relationship exists between MHC and autoimmune diseases. A link between HLA types and autoimmune diseases has been suggested by studies in families and population with disease vis a vis normal healthy subjects.

RELATED;

1. THE MAJOR HISTOCOMPATIBILITY COMPLEX

2. THE HUMAN LEUKOCYTE ANTIGEN

3. AUTOIMMUNE DISEASES

4.  ADAPTIVE IMMUNITY

REFERENCES

ALBUM OF MEDICAL MICROBIOLOGY

ALBUM OF MEDICAL MICROBIOLOGY:

1.  Neisseria gonorrhoeae

2.  Salmonella typhi

3.  Helicobacter pylori

4.  Vibrio cholerae:  This is the causative organism for the deadly diarrheal disease cholera, prevalent in developing countries with rampant poor sanitation and shortage of water.

RELATED;

1.  Album of biochemistry

2.  Album of Pharmacology, therapeutics and toxicology

3.  Album of medical conditions