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”).

 

RELATED;

1.  QUININE AND QUINIDINE

2.  ARTEMESININ COMBINATION THERAPIES

3.  SALFONAMIDES

4.  MEDICAL MICROBIOLOGY

5.  PHARMACOLOGY AND THERAPEUTICS

REFERENCES

HEPATIC FAILURE

 

INTRODUCTION:  hepatic failure is the clinical syndrome of sudden and severely impaired liver function in a previously healthy person. It is characterized by the development of first symptoms or jaundice within 8 weeks of the onset of disease. Three categories are frequently cited: hyperacute, acute, and subacute. The hepatic lesion is potentially reversible, and survival rates are approximately 20% to 50%, depending greatly on the cause of liver failure. Those who do not survive die of massive hepatocellular injury and necrosis.

CAUSES OF LIVER FAILURE:  Viral hepatitis a common cause; other causes include toxic drugs and chemicals, metabolic disturbances, and structural changes.

CLINICAL MANIFESTATIONS:  Jaundice and profound anorexia.  Often accompanied by coagulation defects, renal failure and electrolyte disturbances, cardiovascular abnormalities, infection, hypoglycemia, encephalopathy, and cerebral edema.

MANAGEMENT:  Liver transplantation (treatment of choice).  Blood or plasma exchanges. Liver support systems, such as hepatocytes within synthetic fiber columns, extracorporeal liver assist devices, and bioartificial liver, until transplantation is possible.

 

RELATED;

1.  JAUNDICE

2. REAL FAILURE

3. HYPOGLYCEMIA

4. EDEMA

5.  ANATOMY AND PHYSIOLOGY OF THE HUMAN LIVER

6.  FUNCTIONS OF THE LIVER

REFERENCES

RIFAMPIN

  

INTRODUCTION:  Rifampin is a semisynthetic derivative of rifamycin, an antibiotic produced by Streptomyces mediterranei. It is active in vitro against gram-positive and gram-negative cocci, some enteric bacteria, mycobacteria, and chlamydiae.

MECHANISM OF ACTION: Rifampin binds to the β subunit of bacterial DNA-dependent RNA polymerase and thereby inhibits RNA synthesis.  We should therefore say it is an antimetabolite but to be precise, it is an RNA synthesis inhibitor.

RESISTANCE TO RIFAMPIN: Resistance results from any one of several possible point mutations in rpoB , the gene for the β subunit of RNA polymerase. These mutations result in reduced binding of rifampin to RNA polymerase. Human RNA polymerase does not bind rifampin and is not inhibited by it.

SPECTRUM OF ACTIVITY:  Rifampin is bactericidal for mycobacteria. It readily penetrates most tissues and penetrates into phagocytic cells. It can kill organisms that are poorly accessible to many other drugs, such as intracellular organisms and those sequestered in abscesses and lung cavities.

PHARMACOKINETICS:  Rifampin is well absorbed after oral administration and excreted mainly through the liver into bile. It then undergoes enterohepatic recirculation, with the bulk excreted as a deacylated metabolite in feces and a small amount excreted in the urine. Dosage adjustment for renal or hepatic insufficiency is not necessary. Usual doses result in serum levels of 5–7 mcg/mL. Rifampin is distributed widely in body fluids and tissues. The drug is relatively highly protein bound, and adequate cerebrospinal fluid concentrations are achieved only in the presence of meningeal inflammation.

CLINICAL USES:  Mycobacterial Infections: Rifampin, usually 600 mg/d (10 mg/kg/d) orally, must be administered with isoniazid or other antituberculous drugs to patients active tuberculosis to prevent emergence of drug-resistant mycobacteria. In some short-course therapies, 600 mg of rifampin is given twice weekly.  Rifampin, 600 mg daily or twice weekly for 6 months, also is effective in combination with other agents in some atypical mycobacterial infections and in leprosy.  Rifampin, 600 mg daily for 4 months as a single drug, is an alternative to isoniazid for patients with latent tuberculosis who are unable to take isoniazid or who have had exposure to a case of active tuberculosis caused by an isoniazid-resistant, rifampin-susceptible strain.

OTHER INDICATIONS: Rifampin has other uses in bacterial infections. An oral dosage of 600 mg twice daily for 2 days can eliminate meningococcal carriage. Rifampin, 20 mg/kg/d for 4 days, is used as prophylaxis in contacts of children with Haemophilus influenzae type b disease. Rifampin combined with a second agent is used to eradicate staphylococcal carriage. Rifampin combination therapy is also indicated for treatment of serious staphylococcal infections such as osteomyelitis and prosthetic valve endocarditis.

ADVERSE REACTIONS:  Rifampin imparts a harmless orange color to urine, sweat, and tears. Occasional adverse effects include rashes, thrombocytopenia, and nephritis. Rifampin may cause cholestatic jaundice and occasionally hepatitis, and it commonly causes light-chain proteinuria. If administered less often than twice weekly, rifampin may cause a flu-like syndrome characterized by fever, chills, myalgias, anemia, and thrombocytopenia. Its use has been associated with acute tubular necrosis. Rifampin strongly induces most cytochrome P450 isoforms (1A2, 2C9, 2C19, 2D6, and 3A4), which increases the elimination of numerous other drugs including methadone, anticoagulants, cyclosporine, some anticonvulsants, protease inhibitors, some non-nucleoside reverse transcriptase inhibitors, contraceptives, and a host of others. Co-administration of rifampin results in significantly lower serum levels of these drugs.

 

RELATED;

1.  GRAM NEGATIVE BACTERIA

2. GRAM POSITIVE BACTERIA

3. ETHAMBUTOL

4.  ISONIAZID

5.  TUBERCULOSIS

REFERENCES

PARASYMPATHOLYTICS

 

INTRODUCTION:  Drugs that block the action of Acetylcholine are known by a number of names, including anticholinergics, cholinergic blockers, muscarinic antagonists, and parasympatholytics.  Although the term anticholinergic is most commonly used, the most accurate term for this class of drugs is muscarinic antagonists, because at therapeutic doses, these drugs are selective for Ach muscarinic receptors and thus have little effect on Ach nicotinic receptors.

PHARMACODYNAMICS:  Anticholinergics act by competing with Ach for binding muscarinic receptors. When anticholinergics occupy these receptors, no response is generated at the neuroeffector organs. Suppressing the effects of Ach causes symptoms of sympathetic nervous system activation to predominate. Most therapeutic uses of the anticholinergics are predictable extensions of their parasympathetic-blocking actions: dilation of the pupils, increase in heart rate, drying of secretions, and relaxation of the bronchi.

THERAPEUTIC USES:  1. GI disorders:  These agents decrease the secretion of gastric acid in peptic ulcer disease. They also slow intestinal motility and may be useful for reducing the cramping and diarrhea associated with irritable bowel syndrome. 

2. Ophthalmic procedures:  Anticholinergics may be used to cause mydriasis or cycloplegia during eye procedures.

3. Cardiac rhythm abnormalities:  Anticholinergics can be used to accelerate the heart rate in patients experiencing bradycardia.

4. Preanesthesia:  Combined with other agents, anticholinergics can decrease excessive respiratory secretions and reverse the bradycardia caused by general anesthetics.

5. Asthma:  A few agents, such as ipratropium, are useful in treating asthma, because of their ability to dilate the bronchi.

6. Overactive bladder:  Anticholinergics treat urinary retention and incontinence.

7. Degenerative nervous system application:  Anticholinergics are used to treat patients who have Parkinson’s disease and whose main symptom is tremor. The prototype drug, atropine, is used for several additional medical conditions due to its effective muscarinic receptor blockade. These applications include reversal of adverse muscarinic effects and treatment of cholinergic agent poisoning, including that caused by overdose of bethanechol, cholinesterase inhibitors, or accidental ingestion of certain types of mushrooms or organophosphate pesticides.

 

RELATED;

1.  ACETYLCHOLINE

2.  CHOLINOMIMETICS

3.  GENERATION OF A NERVE IMPULSE

4.  DIVISIONS OF THE CENTRAL NERVOUS SYSTEM

5.  ATROPINE

REFERENCES

ALUMINUM HYDROXIDE

Therapeutic Class: Antiheartburn agent

Pharmacologic Class: Antacid

ACTIONS AND USES:  Aluminum hydroxide is an inorganic agent used alone or in combination with other antacids. Combining aluminum compounds with magnesium, increases their effectiveness and reduces the potential for constipation. Unlike calcium-based antacids that can be absorbed and cause systemic effects, aluminum compounds are minimally absorbed.  Their primary action is to neutralize stomach acid by raising the pH of the stomach contents.

Unlike H2-receptor antagonists and PPIs, aluminum antacids do not reduce the volume of acid secretion. They are most effectively used in combination with other antiulcer drugs for the symptomatic relief of heartburn due to PUD or GERD.

ADMINISTRATION ALERTS:  Administer aluminum antacids at least 2 hours before or after other drugs because absorption could be affected.  Pregnancy category C

ADVERSE EFFECTS: When taken regularly or in high doses, aluminum antacids cause constipation.

At high doses, aluminum products bind with phosphate in the GI tract and long-term use can result in phosphate depletion. Those at risk include those who are malnourished, alcoholics, and those with renal disease.

Contraindications: This drug should not be used in patients with suspected bowel obstruction.

INTERACTIONS:  Drug–Drug: Aluminum compounds should not be taken at the same time as

other medications, because they may interfere with absorption.

 

RELATED;

1.  PEPTIC ULCER DISEASE

2.  CONSTIPATION

3.  HISTAMINE 2 RECEPTOR BLOCKERS

4.  DIARRHEA

5.  PHARMACOLOGY AND THERAOEUTICS

REFERENCES

 

SEXUALLY TRANSMITTED DISEASES (STDS)

INTRODUCTION: Diseases can be transmitted in many ways and among them we have sexual activities, blood transfusion, intravenous drug use and pregnancy related means as seen in the picture above.  Sex intercourse is one of the vertical routes from which many blood borne infections can be transmitted. Sexually transmitted diseases (STDs) are those in which the pathogen is acquired during sexual activity. Most are caused by bacteria or viruses.  In our discussion here, we are looking at some of the most common infections transmitted and the microorganisms responsible for such infections.

GONORRHEA: This is caused by the bacterium Neisseria gonorrhoeae. Infected men have urethritis with painful and frequent urination and pus in the urine. Women are often asymptomatic, and the bacteria may spread from the cervix to other reproductive organs (pelvic inflammatory disease [PID]). The use of antibiotics in the eyes of all newborns has virtually eliminated neonatal conjunctivitis acquired from an infected mother. Gonorrhea can be treated with antibiotics, but resistant strains of the bacteria complicate treatment. Despite this, the number of reported cases of gonorrhea has been decreasing in recent years. Pelvicinflammatory disease: Neisseria: Antimicrobial drug resistance

SYPHILIS: This is caused by the bacterium Treponema pallidum. Although syphilis can be cured with penicillin, it is a disease that may be ignored by the person who has it because the symptoms may seem minor and often do not last long. If untreated, however, syphilis may cause severe or even fatal damage to the nervous system and heart. In the last few years the number of reported cases of syphilis has been decreasing. Syphilis

GENITAL HERPES: This is caused by the virus herpes simplex (usually type 2). Painful lesions in the genital area are the primary symptom. Although the lesions heal within 5 to 9 days, recurrences are possible, perhaps triggered by physiological stresses such as illness. Although herpes is not curable at present, medications have proved useful in suppressing recurrences. It is estimated that 2 million new cases of genital herpes occur every year. Virology

Neonatal herpes is infection of a newborn during passage through the birth canal. The infant’s immune system is too immature to control the herpes virus, and this infection may be fatal or cause brain damage. A pregnant woman with a history of genital herpes may choose to have the baby delivered by cesarean section to avoid this possible outcome.

CHLAMYDIAL INFECTION: This is caused by the very simple bacterium Chlamydia trachomatis. This is one of the most prevalent STDs in developed countries. Infected men may have urethritis or epididymitis.  Women often have no symptoms at first but may develop PID, which increases the risk of ectopicpregnancy. Infants born to infected women may develop conjunctivitis or pneumonia. Chlamydial infection can be treated successfully with antibiotics such as erythromycin or azithromycin.

RELATED;

1. AZITHROMYCIN  

2. ELECTILE DYSFUNCTION DRUGS

3.  TREPONEMA PALLIDUM

REFERENCE

CONSEQUENCES OF COVID 19 INDUCED LOCKDOWN

CONSEQUENCES OF COVID 19 INDUCED LOCKDOWN