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

REPLICATION AND MULTIPLICATION OF HIV IN THE HUMAN BODY AND IT'S PREVENTIVE MEASURES

 

OBJECTIVES OF THE DISCUSSION:  By the end of this presentation, the medical student/reader will be able to;

1.  Describe a brief history in relation to the emerging of HIV

2.  Outline the way through which HIV virus is contacted

3.  Distinguish between the people at high risk of developing HIV compared to the rest of the community.

4.  Describe the infectious cycle of HIV

5.  Outline the goals of antiretroviral drugs and finally

6.  Outline the preventive measures that can be employed to combat HIV

REPLICATION AND MULTIPLICATION OF HIV IN THE HUMAN BODY:  The human immune virus and it's associated illness HIV/AIDS has been one of the most troublesome medical conditions since the early 70s and 80s to date.  In Uganda, this disease is said to have started from South Western part of the country in The district of Rakai, and spread across the country and abroad.  Although this illness initially was regarded as a curse and the community perceived it as a cultural and supernatural phenomenon, and lots of myths and misconceptions were developed for the condition, scientific investigations proved that the disease was, and is actually viral by origin and several drugs have been developed against it and they have proved to be effective in reducing the burden of the disease.  Currently 1000s of individuals are taking Antiretroviral drugs to cub the spread of HIV and it's related complications and generally there is an improvement in the quality of life for those living with HIV/AIDS.  However, the disease still posses a great burden and in recent epidemiological studies, it is indicated to have reversed the predicted trends towards it's prevention to spread especially true, in the previous Millennium Development goals (MDG 2015) were it did the reversal.  We are currently watching the next move with Sustainable development goals 2030. 

The brief microbiology shows that, the virus occurs in two strains namely; HIV 1 which is the commonest in the tropical areas of Eastern Africa, and HIV 2 which is more common in parts of West Africa.  Several sources state it that this disease has more prevalence in African countries however evidence shows that the disease is affecting all the continents at varying percentages.  In this article we are going to look at the way, this deadly predator enters the human body and and be able to multiply.  If you have not been following us, you can also read the discussion below about it's progression to AIDS;  HIV progression to AIDS

WAYS THROUGH WHICH THE VIRUS IS ACQUIRED:  First, let us look at the most common ways of exposure to HIV infection.  Although many people thing the direct way we can get HIV is via copulation, this is actually a minor route for many because the transmission via that route can be prevented and or modulated.  Ok let's take it as number one for that matter because it is the most commonly known and visible to everyone on the go;

1.  Unprotected sex intercourse: Having sex without use of a condom is one way and this is especially true due to possibilities of sores in the genitals of any or all the partners.  HIV is not confined to male-female copulation alone but can also result from oral sex and homosexual practices as well.  Our greatest fear with unprotected sexual intercourse, lies behind the fact that many couples are negligent in testing themselves before any issues happen and for those that endeavor to test themselves, the idea of sexual network is still a major concern.

2.  Mother to child transmission:  There are many ways a pregnant mother can transmit HIV to hear newly born baby if the delivery process is not conducted well.  During delivery of a baby, there are chances that if the process is not handled with care, an HIV positive mother can pass on the virus to her newborn baby.  This is because, the blood spilling is much during the delivery procedures and therefore require attention from a trained medical personnel.

Delivery is not the only way HIV can be transmitted to a newborn, there are many other ways that we shall be seeing in our next discussions concerning the Mother-to-child-transmission of HIV.

3.  Sharing of equipment such as blade, injection needles and other medical equipment:  This can happen both between person to person in the community settings, and between a patient, and a careless medical workers.  As the the sharing of equipment in fact may be intended especially in the case of a resource limited setting, there is a need to ensure the HIV status between the sharing partners.  We are lucky nowadays the coming of technology and industrialization is putting us in plenty of almost everything we may need but I witnessed in the early 90s, an injection needle being boiled before being used to administer drugs to another patient.

4.  Via blood transfusions:  The other possibility of acquiring HIV is via being transfused with blood from an HIV positive blood donor.  This in fact does not only transmit HIV alone but also, other blood borne diseases including but not limited to Tuberculosis and hepatitis.  I talked more about this in my article about; Blood transfusion and the human body.

5.  Inappropriate medical practices:  Inappropriate medical/clinical practices are some of the leading transmission ways of exposing health workers to HIV infection.  These include but not limited to; handling patients and hospital waste without donning gloves, frequent accidental needle pricks, injuries from used medical equipment and accidental exposure to infectious fluids such as amniotic fluids during labor assistance.  It happened to once during my clinical years way back in 2012 while attending and assisting a mother to deliver in labor suit, when I did not have a face mask and as I was doing the procedures, I oriented myself poorly that when the membranes raptured, the amniotic fluids splashed into my eyes.  It was more frustrating to know that we had already tested the mother and she was HIV positive and actively on ART.  Likely enough, it was such a time that Post-exposure prophylaxis (PEP) was already implemented and I was one person to benefit from it after the scenario.

THE FOLLOWING INDIVIDUAL ARE AT RISK OF CONTACTING HIV:  When we talk of a risk we mean; these are individuals with increased chances of contacting HIV virus compared to the rest of the population.

1.  Homosexuals

2.  Intravenous drug abusers

3.  Couples having unprotected sexual intercourse before screening.

4.  Individuals with multiple sexual partners

5.  Commercial sexual workers

THIS IS WHAT HAPPENS WHEN HIV ENTERS YOUR BODY:  Now that we have seen the ways we can contact the HIV, let us see what actually happens after the virus has entered the body.  There is one thing that is special with this virus, it only has receptors on the type of immune cell known as T-cell or in simple terms, the CD4 cell.  The surface of the CD4 cell, lies surface types of glycoproteins that facilitate it's entry inside the cell where it will be able to replicate and multiply.

The other important aspect of the HIV virus is that it does not curry out it's own activities but instead, uses cellular metabolic pathways to carry out it's activities.  In fact the HIV virus is special in it's own ways that; it reverses the normal genetic pathways where the DNA molecule multiplies into two in a process known as replication, and produce RNA in a process known as transcription, which produces proteins in a process we call translation.  This is known as the "Central dogma of microbiology".

To have a brief look at the individual virus, we call it a viral particle and with it, comes a pack of 2 viral RNA strands, the enzymes integrase, reverse transcriptase, and protease all enveloped in a capsule. Now, as the viral particle enters the human CD4 cell, the capsule is opened and the viral components mentioned above are poured into the cytoplasm of the human CD4 cell.  The viral components now starts to give the CD4 cell orders, to synthesize, a viral DNA portion from the available viral RNA strands using cellular nucleotides.  This is the process known as, reverse transcription.  If you are not familiar with some of the terms we are using here, never mind the microbiological and biochemistry feel free to skip to the next part of the discussion.  This is especially true for non medical personnel reading this blog.  Also, in my previous discussions I looked at some of the molecules I am mentioning here and you can use the links below to read about them; Deoxyribonucleic acid (DNA), Ribonucleic acid (RNA), Nucleotides.

We stopped at the production of a viral DNA portion from viral RNA stands and now at this stage, the enzyme viral integrase incorporates this viral genome into the CD4 or human DNA stand or genome.  The result of this, is a lengthy DNA molecule of the CD4 cell, containing portions of the viral genetic information.  Remember all this is happening on the expense of the cellular energy and now when the process of DNA replication starts, viral portions will as well be replicated, yielding more viral RNA strands and subsequent viral proteins for the maturation and assembly of new viral particles.  Once this is done, the newly formed viral particles will go out of this CD4 cell by the process of exocytosis, and infest more and more CD4 cells and cycle continues.  I already discussed the process through which HIV infest and destruct the CD4 cells in a separate discussion you can find it in the link below;  Invasion of Human CD4 cell by the human immune virus.

THESE ARE THE TARGETS OF ANTIRETROVIRAL DRUGS ON THE HIVVIRUS:  Now that we have seen the way the virus enter and disrupt the cellular functioning, the drugs that are used to reduce on this burden also known as Antiretroviral drugs (ARVs) target special processes of the viral replication cycle as follows;

1.  Some will be able to inhibit the virus from entering the CD4 cell at the plasma membrane level and this class of drugs is known as Fusion inhibitors.

2.  The other class will inhibit the production of viral DNA from viral RNA strands usung cellular nucleotides and we shall call those, Nucleoside Reverse Transcriptase inhibitors (NRTIs).

3.  The third class will be able to inhibit the actual enzyme involved in production of the viral DNA from the viral RNA strands, and remember from the beginning the viral particle comes equipped with this enzyme; Reverse transcriptase.  Then we shall call the group of drugs falling here, Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs).

4.  The fourth class will be effective by inhibiting the incorporation of the formed viral DNA portion into the human or CD4 DNA strand, by affecting the action of the enzyme integrase, responsible for that process.  We shall therefore call these class of drugs, Integrase Inhibitors.

5.  The final or one of the last class, will be able to inhibit the maturation of the formed viral particles and therefore they will not be able to go out of the CD4 cell to affect other CD4s or if they go out, they will be be immature and therefore with no virulence.  These drugs will be interfering with the enzyme Protease and we shall call the class, Protease inhibitors.

In a separate discussion, we shall be able to look at some of specific drug names as they appear in all the 5 sub classes mentioned above, and the possible combinations that causes synergism in order for the therapeutic regimen prescribed to be effective but before we leave this section of the discussion, don't forget to read about general classification of drugs from the link below; Classification of pharmaceutical products and drugs.

THIS IS THE WAY HIV CAN BE PREVENTED:  Now let us come up with the preventive measures of HIV.  First, and foremost, for mature adults the most trusted and reliable means focuses on regular testing and diagnosis for those looking for sexual partners.  The most outstanding goal here, is to have safe sexual practices as long as the couple tests HIV negative, and prevent the consequences that may result from discordancy.  The next strategy to that will be avoiding multiple sexual partner or as the campaign says; get off the sexual network and increase trustworthiness among the couples.  If all these may not be possible all the time then at least maximize the proper use of condoms.  The preventive measure on the same issue is ensuring safe sexual practices like we saw at the beginning that or sex and homosexuality can as well predispose you to contact HIV.

The other preventive measure will be looking as good and safe clinical practices including proper use of medical gears, emphasis on Standard Operating Procedures and proper disposal of medical wastes.  For the health workers, the Prevention of Mother to Child Transmission (PMTCT) is already on the go and documentations from researchers indicate a reduced number of newborns to HIV positive mothers however, we will have a need to address more and more the practice of pregnant mothers especially from rural setting, to deliver from health facilities and get assisted by trained medical personnel.  In some of our next discussions, we shall be talking about what has been put forward to reduce the incidence of HIV in newborns and those affected with HIV during and following birth.

CONCLUSION:  HIV is one of the current global burdens with no radical cure established yet.  It's prevalence is higher in developing countries especially sub Saharan Africa and it continues to spread, reversing the expected trends from many Governments.  It was very much deadly in the 80s and 90s but the coming of antiretroviral drugs, there is some relief for the last two decades.  Many families now are living with HIV and on drugs, but they are living happy life following counseling and compliance to the medications.  The documented mortality rates that happened in the 80s before the drugs were available, is now far reduced and there is hope that with increasing discovery of more and more therapeutic regimens for HIV will finally eliminate the disease and we live an HIV free ecosystem.

RELATED;

1.  HIV PROGRESSION TO AIDS

2.  BLOOD DONATION, TRANSFUSION AND THE HUMAN BODY

3.  TUBERCULOSIS

4.  HEPATITIS

5.  DNA, THE GENETIC MATERIAL

6.  RIBONUCLEIC ACID, RNA, THE GENETIC MATERIAL

7.  NUCLEOTIDE, THE BUILDING BLOCKS OF RNA AND DNA

8.  INVASION OF THE HUMAN CD4 CELLS BY THE HUMAN IMMUNE VIRUS

9.  CLASSIFICATION OF DRUGS

REFERENCES

NOSOCOMIAL INFECTIONS

NOSOCOMIAL INFECTIONS:  On our way to clinical setting, we always have chief complaints.  So we are seeking advice from a trained medical personnel from either a Public or Private Health Centre or Clinic, Hospital or in a health outreach service.  Whether our general problem is diagnosed or not, it's severity will predetermine our admission or immediate discharge after the medical interventions are done.  Usually while in the hospital setting, patients usually suffer from diseases they did not come with, or they were not present and diagnosed at the time of admission and we call these nosocomial or hospital acquired infections.  We may actually look at it in one way but if you are very observant, nosocomial infections can affect patients, health workers and non medical stuff attendants in the hospital settings.

   

Some of the most common infections acquired include but not limited to respiratory tract infections such as pneumonia, flu and cough, skin infection, conditions that affect the gastrointestinal tract and tropical disease. In this discussion, we are going to look at the causes of such infections, their transmission and preventive measures employed in hospital setting to overcome them.

THE ORIGIN OF NOSOCOMIAL INFECTIONS:  Emergency of hospital acquired infections can depend on three major factors as described below depending on the possible origin of infections;

a)  Health worker related issues:  Some of the causes of hospital acquired infections will be related to health workers and the health setting it's self.  First, when patients come to the health facility, they should be oriented about the goings and makeup of that specific clinical setting.  This is to ensure that any medical procedure is done correctly and any medical waste is disposed off the right way.  Sometimes this does not happen and you find the patients are doing things according to their own understanding and confusion, on the expense of health workers and administrators failure to orient them.  A good example of this is the improper disposal of medical waste that maybe very infectious in bins and areas where they are hazardous to the hospital population.  This can lead transmission of infections not only to patients but also to hospital waste handlers.

The other way health workers are responsible for hospital acquired infections is via negligence and poor medical practices.  This is uncommon but we can not forget to talk about it.  It should be noted that before performing any invasive procedure on the patient, safety precautions must be put in place.  These include protective gears to the patient and or the medical work especially disinfecting and use of sterile equipment.  Once this is not done, the origin of blood indwelling microbes will not be preventable and one of the most common nosocomial infection in that respect will be sepsis.

Although the fear and anxiety related to illness can barely be eliminated, the patient should have some feeling of comfort for the period they are supposed to stay with in the facility and utilize the available resources with no fear.

b)  Patient related issues:  Although the health worker contributes a lot towards emergency of hospital acquired infections, the biggest percentage of root causes come from the patients themselves.  Some of the patient related issue that you don't want to under look include misuse of hospital facilities and contamination of hospital linen, fomites and aiding instruments.  This superimposed by ignorance about disinfection, sterilization and proper handling of medical material in the hospital settings is the leading cause of transmission of the most common infectious agents responsible for hospital acquired infections.

c)  Environmental issues:  The nearby environment also plays a role in development of hospital acquired infections.  First, the health facility is the collection of many patients with different illnesses and therefore anyone admitted there is exposed.  With inevitable human interactions, diseases will easily be able to get access into the nearby population.

The other environmental issue that may play a role in development of hospital acquired infections is presence of disease-carrying vectors.

PREVENTION OF NOSOCOMIAL INFECTIONS:  Some of the ways we can prevent nosocomial infections are universal and they rotate on good hygiene and proper practicing methods for health workers.  Now with the reinforcement of Standard Operating Procedures (SOPs) following the COVID 19 pandemic, hospital acquired infections can even be prevented more and more. 

CONCLUSION:  Hospital acquire infections can as well be contacted from our homes and communities but the difference here is that, exposure in the hospital settings is as good as in prisons, armed forces barracks, and any other long term stationed gathering.

RELATED;

1.  THE HUMAN MICROBIOME

2.  NORMAL FLORA OF THE HUMAN BODY

3.  DYNAMICS OF THE HUMAN BODY-SYSTEMS MAKE-UP

4.  HOSPITAL ACQUIRED PNEUMONIA

5.  DYNAMICS OF INFECTIOUS DISEASES

6.  CAUSATIVE AGENTS OF HOSPITAL ACQUIRED INFECTIONS

VACCINES

INTRODUCTION: Vaccines have always been developed and used for ages so far. The purpose of vaccines is to prevent disease for known infectious agents and following thorough scientific demonstration and investigations in animal species such as mice, rats, rabbits among others, safer and effective vaccines are developed for prevention of various intended diseases. The safer and effectively developed vaccine against disease X is then used in the human populations to eradicate the disease.

COMPOSITION OF VACCINES: A vaccine contains an antigen that the immune system will respond to, just as it would to the actual pathogen. To look at the antigen more closely, it will have some resemblance to the intended pathogen in order to be able to stimulate the immune system.

TYPES OF VACCINES: The types of vaccine antigens are;

1. A killed or weakened also known as attenuated pathogen,

2. Part of a pathogen such as a bacterial capsule, or an inactivated bacterial toxin called a toxoid.

PATHOPHYSIOLOGY: Because the vaccine itself does not cause disease with very rare exceptions, the fact that antibody production to it is slow is not detrimental to the person. The vaccine takes the place of the first exposure to the pathogen and stimulates production of antibodies and memory cells. On exposure to the pathogen itself, the memory cells initiate rapid production of large amounts of antibody, enough to prevent disease.

EXAMPLES OF VACCINES: We now have vaccines for many diseases. The tetanus and diphtheria vaccines contain toxoids, the inactivated toxins of these bacteria. Vaccines for pneumococcal pneumonia and meningitis contain bacterial capsules. These vaccines cannot cause disease because the capsules are non-toxic and nonliving; there is nothing that can reproduce. Influenza and rabies vaccines contain killed viruses. Measles and the oral polio vaccines contain attenuated (weakened) viruses. Although attenuated pathogens are usually strongly antigenic and stimulate a protective immune response, there is a very small chance that the pathogen may regain its virulence and cause the disease with proper clinical practice.

RELATED;

1.  ACTIVE IMMUNISATION

2.  BCG VACCINATION

3.  PASSIVE IMMUNISATION

4.  ORGANS OF THE IMMUNE SYSTEM

5.  INNATE IMMUNITY

REFERENCES

HUMAN PAPILLOMAVIRUSES

 

INTRODUCTION: Papillomaviruses cannot be grown in cultures and existence of a large number of distinct human papillomaviruses became evident only after the development recombinant DNA technology. Different types of human papillomaviruses (HPV) are associated with lesions of specific morphology and at specific anatomic sites some of which include the cervix.

MORPHOLOGY: The virion is non-enveloped and has a diameter of 55 nm, icosahedral symmetry and 72 capsomers. The viral genome is a double stranded, circular DNA molecule with molecular weight of 5.2 million daltons. The viral capsid proteins consist of a major polypeptide and a number of minor polypeptides. Purified virion contains four histones of host origin.

PATHOGENESIS: Human papillomaviruses infect only epithelium of skin and mucous membranes. The virus probably infects cells of the lower layers of the epithelium which undergo proliferation and form the warts. Histologically, a wart is localised epithelial hyperplasia with a defined boundary and an intact basement membrane. Clinically warts can be of various types.

DIAGNOSIS: It is essentially clinical. History can confirm the diagnosis of warts but it does not indicate the type of HPV responsible. No serological tests are available for virus identification. Human papillomaviruses cannot be grown in culture. A broadly cross-reactive genus-specific antiserum is available, which is capable of recognising capsid antigen of all human and animal papillomaviruses by immunoperoxidase or immunofluorescent tests. Identification of viral genotype is possible by DNA hybridisation methods.

TREATMENT: Most skin and genital warts regress spontaneously. The patient seeks treatment for cosmetic reasons, pain, discomfort, and disability depending on the location and size of warts. The treatment includes application of caustic agents such as podophyllin and salicylic acid, cryotherapy, surgical removal, and antimetabolites such as 5-fluorouracil.

RELATED;

1.  HUMAN IMMUNE VIRUS

2.  INFECTION BY THE MUMPS VIRUS

3.  VIRAL HEPATITIS

4.  RETROVIRUSES

REFERENCES

INFLUENZA

INTRODUCTION: Influenza is an acute viral disease that causes worldwide epidemics every 2 to 3 years with a highly variable degree of severity. The virus is easily spread from host to host through droplet exposure. Previous infection with influenza does not guarantee protection from future exposure. Mortality is probably attributable to accompanying pneumonia which maybe viral or superimposed bacterial pneumonia, and other chronic cardiopulmonary condition.

MANAGEMENT: Goals of medical and nursing management include relieving symptoms, treating complications, and preventing transmission.

PREVENTION: Annual influenza vaccinations are recommended for those at high risk for complications of influenza. These include people older than 50 years, children 6 to 59 months of age, pregnant women, residents of extended care facilities, and those with chronic medical diseases or disabilities. In addition, health care providers and household members of those in high-risk groups should receive the vaccine to reduce the risk of transmission to people vulnerable to influenza sequelae.

RELATED;

1. SYMPTOMATIC MANAGEMENT OF PATIENTS

2.  EBOLA VIRUS DISEASE

3.  IMMUNISATION

REFERENCES

CANDIDIASIS

INTRODUCTION:  This is a fungal infection that is common especially in immunocompromised patients.  Usually fungi microbes are not a big burden in immunocompetent individuals and if the do infect an individual, in most cases they will be asymptomatic.  The commonest of these fungal species is Candida albicans.  Other important species include; Candida tropicalis, C. pseudotropicalis, C. brumptii, C. parapsilosis, C. guilliermondii, C. krusei.  

MORPHOLOGY AND REPRODUCTION:  The thallus of Candida consists of yeast cells and pseudohyphae. They reproduce by budding, ferment a number of sugars and assimilate nitrogen.  Microscopic examination of pathological material shows round or oval yeast cells in the process of budding and often exhibiting pseudohyphae.

PATHOGENESIS:  Under normal conditions this fungus is not pathogenic. Many factors predispose to pathogenic effect and these include the following;

1.  Impaired immune defences,

2. Pregnancy

3. Spontaneous hormonal

4. Menopause changes

5. Premature birth

6. Use of Corticosteroids

7. Immunosuppression

8. Long-term antibiotic therapy

9. Oral contraceptives

10. Diabetes mellitus

11. Pre-existing lesions of skin

CLINICAL FEATURES:  A variety of infections are caused by Candida species though it is an opportunistic fungus.  In addition to general predisposing factors, following local conditions also predispose to this infection: Chemical, mechanical or biological irritants, Reduced salivation, Digestive disorders, Remnants of milk left fermenting in the mouth of infants.

LABORATORY DIAGNOSIS:  Collection of Infected Material Skin or nail scrapings, mucous patches from the mouth, vagina or anus, sputum, blood, CSF or faeces may be collected for diagnosis in the laboratory. The material should be collected in sterile containers or as smears on slides.

TREATMENT:  Predisposing factors should be eliminated. The affected area should be kept dry.  Topical application of nystatin and systemic treatment with Amphotericin B, oral ketoconazole and fluconazole is effective.

 

RELATED;

1.  INTRODUCTION TO FUNGI

2.  AMPHOTERICIN B

3.  OPPORTUNISTIC MYCOSES

REFERENCES

ENTAMOEBA HISTOLYTICA

 

INTRODUCTION:  Entamoeba histolytica is significant as the causative agent of the worldwide occurring entamebosis, a disease particularly prevalent in warmer countries. The vegetative stages also known as trophozoites of E. histolytica live in the large intestine and form encysted stages also known as cysts, that are excreted with feces.  The infection is transmitted by cysts from one human to another. The trophozoites of E. histolytica can penetrate into the intestinal wall and invade the liver and other organs hematogenously to produce clinical forms of amebosis, most frequently intestinal ameboses also termed “amebic dysentery” and hepatic amebosis frequently called “amebic liver abscess”.  Diagnosis of an intestinal infection is primarily confirmed by detection of the parasites in stool. If an invasive, intestinal or extraintestinal infection with E. histolytica is suspected, a serological antibody test can also provide valuable information.

OCCURRENCE AND PATHOGENICITY:  In endemic areas in Africa, Asia, and Central and South America up to 70–90% of the population can be are carriers of E. histolytica. The causative agent of amebosis is the pathogenic E. histolytica.  The trophozoites colonize the large intestine mucosa or lumen. E. histolytica can disseminate to other organs from the intestinal wall, most particularly to the liver. As a result of the destruction of parenchymal cells, small necrotic foci, so-called abscesses, form and gradually become larger and can even affect major portions of the organ.

EPIDEMIOLOGY:  Humans are the reservoirs for E. histolytica. The infection is due to transmission of mature cysts with contaminated foods especially from fruit, vegetables, drinking water or fecally contaminated hands. Flies and cockroaches can function as intermediaries by carrying cysts from the feces of an excretor to foods. The amounts of chlorine normally added to drinking water are insufficient to kill the cysts.

CLINICAL MANIFESTATIONS:  Clinical symptoms can develop as early as two to four weeks after infection with E. histolytica or after asymptomatic periods of months or even years. The acute disease usually begins with abdominal discomfort and episodes of diarrhea of varying duration, at first mushy then increasing mucoid, including blood-tinged, so-called “red currant jelly stools” in which amebas can be detected, including trophozoites containing erythrocytes. In such cases, antibodies are usually present in serum.

Extraintestinal forms:  Extraintestinal forms develop because of hematogenous dissemination of E. histolytica originating in the intestine. The most frequent form is the so-called “liver abscess,” which may develop in some infected persons. Only about 10% of patients with liver abscesses are also suffering from amebic colitis.  

The liver abscess causes remittent fever, upper abdominal pain, liver enlargement, elevation of the diaphragm, general weakness, and other symptoms.  Antibodies are detectable in most cases

THERAPY:  Nitromidazole derivatives are effective against symptomatic intestinal and extraintestinal forms of amebosis. On the other hand, amebicides with only luminal activity are effective against asymptomatic intestinal amebosis.

PREVENTION:  Travelers to endemic areas should decontaminate drinking water by boiling or filtering it, not eat salads, eat only fruit they have peeled themselves and exercise caution when it comes to changing their diet. Chemoprophylactic dugs are not available.

 

RELATED;

1.  PLASMODIUM

2.  BACTERIOLOGY

3.  VIROLOGY

4.  ANTIMICROBIAL AGENTS

5.  PROTOZOA

REFERENCES

TRICHOMONAS VAGINALIS

 

INTRODUCTION:  Trichomonas vaginalis is a frequent flagellate species that occurs worldwide and is transmitted mainly by sexual intercourse. It causes vaginitis in women and urethritis in men.

OCCURRENCE: In average populations of developed countries, infection rates are about 5–20% in women and usually below 5% in men. 

PARASITE, LIFE CYCLE, AND EPIDEMIOLOGY:  Trichomonas vaginalis is a pearshaped protozoon. Five flagella emerge from a basal body at the anterior pole, four freely extend forwards and one extends backwards, forming the outer edge of the undulating membrane, which reaches back only just beyond the middle of the cell. An axial rod made up of microtubules protrudes with its free tip from the posterior end of the cell. The oval cell nucleus lies near the upper pole of the protozoon.

Trichomonads are anaerobic protozoa that possess hydrogenosomes, which are specialized organelles producing H2 as a metabolite. T. vaginalis colonizes the mucosa of the urogenital tract and reproduces by longitudinal binary fission. Trichomonads do not encyst, although rounded, nonmotile forms are observed which are degenerated stages without epidemiological significance.  The parasites are transmitted mainly during sexual intercourse. About 2–17% of female neonates born of infected mothers contract a perinatal infection.

SUSCEPTIBILITY TO DRYNESS AND CHEMICALS:  T. vaginalis is highly labile outside of a host.  Nonetheless, a few trophozoites can survive for up to five hours in the water of non-chlorinated thermal baths and for five minutes to 24 hours in tap water with standard chlorination; they are killed within a few minutes in swimming-pool water with high chlorine concentrations. It is conceivable that infections could be transmitted by wet bathing suits, sponges, towels, etc. as well as acquired from non-chlorinated thermal baths and poorly maintained swimming pools, but there is no evidence showing that these are significant sources of infection.

CLINICAL MANIFESTATIONS:  In women, T. vaginalis primarily colonizes the vaginal mucosa, more rarely that of the cervix. In about 20–50% of cases the infection is asymptomatic, but vaginitis can develop after an incubation period of two to 24 days. The infection results in production of a purulent, thin, yellowish discharge in which trichomonads, pus cells, and bacteria are found.

The parasites also enter the urethra in about 75–90% of cases, where they can also cause an inflammation, but only rarely infect the urinary bladder or uterus. Infections in men are for the most part asymptomatic (50–90%), but they may also cause a symptomatic urethritis, more rarely involving the prostate gland and seminal vesicles as well. Infection does not confer effective immunity. 

DIAGNOSIS:  A fresh specimen of vaginal or urethral secretion is mixed with physiological saline solution and examined under a microscope for trichomonads. The trichomonads are readily recognized by their typical tumbling movements. The round trichomonad forms, by contrast, are hardly distinguishable from leukocytes. Trichomonads can also be identified in smear preparations following Giemsa staining or in an immunofluorescence test with monoclonal antibodies. The most reliable diagnostic results are obtained by culturing specimens in special liquid media.  Other special methods are based on detection of antigen (ELISA) or DNA (PCR).

THERAPY AND PREVENTION:  It is always necessary for both sexual partners to receive treatment. Effective nitromidazole preparations for oral application in women vaginal application include metronidazole, tinidazole and ornidazole.  These substances are contraindicated in early pregnancy. Preventive measures are the same as for other venereal diseases.

 

RELATED;

1.  PLASMODIUM

2. METRONIDAZOLE

3. ALBUM OF PROTOZOLOGY

4. MEDICAL MICROBIOLOGY

5. PHARMACOLOGY AND THERAPEUTICS

REFERENCE

PLASMODIUM

  

INTRODUCTION:  Plasmodium, the causative agent of malaria, the most frequent tropical parasitosis in Sub Saharan Africa and tropics.  The infection is caused by plasmodia including; Plasmodium vivax, P. ovale, P. malariae and P. falciparum transmitted by the bite of Anopheles mosquitoes.

An infection initially presents in nonspecific symptoms including but not limited to; headache, fatigue, nausea, and fever. Untreated malaria especially caused by P. falciparum, can quickly develop to a lethal outcome. Therefore, it is important to obtain an etiological diagnosis as quickly as possible by microscopic detection of the parasites in the blood, and to initiate effective treatment. Prophylactic measures are essential for travelers to regions where malaria is endemic.

MALARIA PARASITES:  Four Plasmodium species infect humans and cause different types of malaria:  Plasmodium vivax is responsible for tertian malaria, Plasmodium ovale for tertian malaria, Plasmodium malariae for quartan malaria, and Plasmodium falciparum for malignant tertian malaria.  These Plasmodium species can be identified and differentiated from each other by light microscopy in stained blood smears during the erythrocytic phase of the infection in humans.

LIFE CYCLE:  The life cycle of malaria plasmodia includes phases of asexual multiplication in the human host and sexual reproduction and formation of sporozoites in the vector, a female Anopheles mosquito. The developmental cycle within the human host is as follows:  

Infection and exoerythrocytic development: Humans are infected through the bite of an infected female Anopheles mosquito that inoculates spindle-shaped sporozoites into the bloodstream. Only a small number of sporozoites are needed to cause an infection in humans (about 10 for P. falciparum).  Within about 15–45 minutes of inoculation, the sporozoites of all Plasmodium species reach the liver in the bloodstream and infect hepatocytes, in which asexual multiplication takes place. In this process, the sporozoite develops into a multinuclear, large schizont (meront) described as a tissue schizont. Following cytoplasmic division 2000 (P. malariae) to 30 000 (P. falciparum) merozoites are produced. This development takes six (P. falciparum) to 15 (P. malariae) days.

Shortly thereafter, the tissue schizonts release the merozoites, which then infect erythrocytes.

Erythrocytic development:  The merozoites produced in the liver are released into the bloodstream where they infect erythrocytes, in which they reproduce asexually.

PATHOPHYSIOLOGY:  Fever is induced when the schizonts burst and when many red blood cells are destroyed at once, causing the typical, intermittent fever attacks (“malarial paroxysm”).  After one or more schizogonic generations, some of the plasmodia in each generation develop into sexual forms, the male microgamonts, and female macrogamonts. These sexual forms (gametocytes) persist for a certain period in the blood, after which those not taken up by blood-sucking Anopheles females die.

CLINICAL MANIFESTATIONS:  The clinical manifestations of malaria are caused by the asexual erythrocytic stages of the plasmodia and therefore commence shortly after parasitemia at the earliest. The incubation periods vary, depending on the Plasmodium species involved, from seven to 35 days after infection. These periods can, however, be extended by weeks or even months, particularly if the infection is suppressed by prophylactic medication.  The clinical manifestations of malaria depend on a number of different factors, above all the Plasmodium species and immune status of the patient. The Plasmodium species with the most pronounced pathogenicity is Plasmodium falciparum, which causes “malignant tertian malaria” (malaria tropica), whereas the other Plasmodium species cause milder forms (“benign malaria”).

 

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3.  SALFONAMIDES

4.  MEDICAL MICROBIOLOGY

5.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

NEISSERIA GONORRHEAE (GONORRHEA)

MORPHOLOGY AND CULTURE: Gonococci are Gram-negative, coffee-bean-shaped cocci that are usually paired. Attachment pili on the bacterial cell surface are responsible for their adhesion to mucosal cells. Gonococci can be grown on moist culture mediums enriched with protein (blood). The atmosphere for primary culturing must contain 5–10% CO2.

PATHOGENESIS AND CLINICAL PICTURE: Gonorrhea is a sexually transmitted disease. The pathogens penetrate into the urogenital mucosa, causing a local purulent infection. In men, the prostate and epididymis can also become infected. In women, the gonococci can also cause salpingitis, oophoritis, or even peritonitis. Gonococci reaching the conjunctival membrane may cause a purulent conjunctivitis, seen mainly in newborn children. Gonococci can also infect the rectal or pharyngeal mucosa. Hematogenously disseminated gonococci may also cause arthritis or even endocarditis.

DETERMINANTS OF THE PATHOGENICITY OF GONOCOCCI: Attachment pili on the surface and the outer membrane protein are responsible for adhesion to cells of the urogenital tract. It also directs the invasion process by means of endocytosis. Immune defenses against granulocytes are based on the outer membrane porin that prevents the phagosome from fusing with lysosomes, resulting in the survival, and proliferation of phagocytosed gonococci in granulocytes. 

The lipo-oligosaccharide (LOS) in the outer membrane is responsible for resistance to complement (serum resistance) as well as for the inflammatory tissue reaction in a manner analogous to the more complexly structured LPS of enterobacteria.

Gonococci can capture iron from the siderophilic proteins lactoferrin and transferrin, accumulating it inside the bacterial cells to facilitate their rapid proliferation.

An IgA1 protease produced by the gonococci hydrolyzes secretory antibodies in the mucosal secretions. The pronounced antigen variability of the attachment pili and the Opa protein make it possible for gonococci to thwart specific immune defense mechanisms repeatedly.

DIAGNOSIS: The method of choice is detection of the pathogens by means of methylene blue and gram staining and culturing. Gonococci are sensitive in cultures and the material must be used immediately after they are obtained to inoculate. Thayer-Martin blood agar with antibiotics added to eliminate accompanying flora, on which medium the cultures are then transported to the laboratory. The identification procedure involves both morphology and biochemical characteristics. Techniques developed recently utilize immunofluorescence or coagglutination methods utilizing monoclonal antibodies to the main protein of the outer membrane, Por. Direct detection in pus and secretion samples is possible using an enzymatic immunosorbence test or detection of gonococcus-specific DNA sequences coding for rRNA using a gene probe.

THERAPY: The agent of choice used to be penicillin G. In recent years, however, the percentage of penicillinase-producing strains has increased considerably all over the world. For this reason, third-generation cephalosporins are now used to treat uncomplicated cases of gonorrhea. They are applied in a single dose (e.g., ceftriaxone, 250–500 mg I.M.). Good results have also been reported with single-dose oral application of fluorinated 4-quinolones (e.g., 0.5 g ciprofloxacin or 0.4 g ofloxacin).

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References