Entamoeba histolytica is a pathogenic protozoan parasite belonging to the genera Entamoeba. Protozoa are distinctly single celled micro-organisms. This protozoan infects primates and humans are adversely affected. Over 50 million people are infected globally. Cats and dogs are transiently infected and also serve as vectors of Entamoeba histolytica and these animals can transmit the parasite to humans. This protozoa has been found in all populations throughoutand it is more prevalent in the tropics and subtropics than the cooler climates. In the western hemisphere, Entamoeba histolytica has been found from Anchorage, Alaska(60°N) to the strait of Magellan(52°S). In the Eastern hemisphere it has been found from Finland(60°N) to Natal, South Africa(30°S) (Guptee, 1999).
It is classified as an intestinal parasite. Intestinal parasites are distinct from other parasites that are blood borne. They possess a unique intestinal stage in their life cycle although they also colonize the lungs, heart and other tissues in the course of their life cycle stages.The mucous and submucous layers of the large intestine form the habitat colonized by trophozoites of Entamoeba histolytica. The intestinal parasites are also harbored by animals and other components of the environment during their life cycle. Intestinal parasites fall into two main classes i.e. protozoa and helminthes. Both types of parasites are characterized by diagnostic stages exhibited in the life cycle of all parasites. This is the cyst stage that occurs during the early life stage and trophozoite stage exhibited during adulthood. The diameter of protozoan cysts is 5-30µm but helminth eggs are generally much smaller. Protozoan cysts unlike helminth eggs can be viewed via a microscope. Cysts need to be concentrated but trophozoites can be viewed directly without concentration (Guptee, 1999)
Protozoa that infect man are mainly transmitted through ingestion of water and food contaminated with feces containing E. histolytica. This infection poses a perennial problem to third world countries in regions where hygiene is wanting. Poverty, poor sanitation and overcrowding are the main factors that contribute to parasite transmission. However developed countries have also reported significant cases of Entamoeba histolytica infection. In the United States about 3% of the population harbors E.histolytica. This parasite is the most common protozoan that is known to infect the gastrointestinal tract. Generally amoeba possess protoplasm that is distinctly clear. The fluidity of the protoplasm allows for the formation of invaginations referred to as pseudopodia. The pseudopodia serve as a means via which the amoeba obtain nutrition via engulfment of red blood cells and other bacteria. The engulfed contents are enclosed into a vacuole upon which enzymes catalyze their digestion and the resultant simple nutrients are utilized by the amoeba (Guptee, 1999).
Entoameba histolytica undergoes binary fission to replicate and subsequently colonize the intestinal tract. It primarily colonizes the colon/large intestine. This parasite actively bores via the bowel’s wall and in the process causes painful ulceration, abdominal pain and dysentery which is mainly manifested via bloody diarrhea. The amoeba can also become integrated into the blood stream and this serves as a mechanism to spread and proliferate in other tissues. Blood from the intestine initially goes to the liver and the parasite causes liver abscesses, the most conspicuous symptom of parasite infestation and disease. The abscesses are not localized in the liver and they also occur in the brain and lungs. Indeed this pathogenic parasite is very potent as it causes dysentery and/or amoebomas after invasion of the intestinal mucosa. In worse case scenarios it causes secondary extra-intestinal lesions and these mainly occur through the systemic circulation and initially affect the liver in most cases
The life cycle of Entamoeba histolytica comprises of two distinct stages i.e. cysts and trophozoite. The cyst is the infective stage whereas the trophozoite is the pathogenic, disease causing stage. The physical appearance of the trophozoite stage is amoeboid and the diameter is 15-30 µM but more pathogenic strains are longer. Under the microscope, the living parasite can be viewed on a warm slide and it exhibits remarkable locomotion. Movement results from long finger-like pseudopodial extensions of the ectoplasm into which the endoplasm flows. The cytoplasm is divisible into a clear translucent ectoplasm and granular endoplasm. Cytoplasm may contain erythrocytes, tissue debris and white blood cells. It has a well defined nuclear membrane, inner line of which is lined with uniform and closely packed fine granules of chromatin. It has one nucleus that has a characteristic central, core karyosome. The extensive, granular endoplasm has remnants of ingested red blood cells (University of Manitoba, 2000).
The pre-cystic stage comprises of a colourless, round/oval organism that is smaller than the trophozoite but larger than the cyst and its size varies from 10-20µM. The endoplasm is free from red blood cells. The pseudopodial activity is sluggish and the nucleus remains intact. The cystic stage occurs in the intestinal lumen under unsuitable conditions. A cyst begins as a unicleated body that divides by binary fission and develops into a binucleated and quadrinuceated structure. The cyst is 6-15µM with clear and hyaline cytoplasm containing oblong bars with rounded ends called chromatoid bars. A distinct glycogen mass is found in the early stages of cyst formation. In a quadrinucleated cyst, both chromatoid bars and the glycogen mass disappear. This is the mature and infective cyst.
The main host of Entamoeba histolytica is the human being and other hosts such as dogs and cats are merely accidental/transient hosts. The cysts are resilient and well adapted to survive under moist conditions for months. However, they are denatured and inactivated by extreme hot and freezing temperatures. Upon ingestion, the cysts produce a trophozoite that has four nuclei. These trophozoites inhabit the intestinal crypts and feed on the host tissue and intestinal contents.The trophozoite undergoes division into four trophozoites and each nucleus migrates into the newly formed trophozoites. These nuclei undergo further subdivision to yield eight trophozoites. The undeveloped trophozoites are transported by the circulatory system to the colon/large intestine. They undergo maturation and undergo subdivision and subsequent replication via binary fission. At this stage the trophozoites are excreted from the host via faeces. In the procees, fecal material is conveyed to the colon where it undergoes dehydration. This dehydration triggers the onset of trophozoite encystment. The food that is undigested is excreted as the trophozoite undergoes condensation to form a pre-cyst which has a spherical shape. There is also secretion of the cyst wall and the nucleus undergoes to form 2 nuclei for an immature cyst and subsequent nuclear division results to the formation of 4 nuclei in a mature cyst. This cyst is resilient to adverse conditions and can tolerate desiccation for a period of 1-2 weeks (University of Manitoba, 2000).
Upon ingestion of food contaminated with the cysts in another host, the parasite undergoes excystation in the intestine and there division to yield 4 trophozoites. These trophozoites are well adapted to the host environment as they secrete proteolytic enzymes that degrade the epithelium of the intestine and thereby facilitating the entry of trophozoites into the host tissue. At this stage, the paraites are very potent as they form abscesses and the parasite is incorporated into the systemic circulation and conveyed by the blood stream to other organs starting with the liver. Extensive destruction is caused at the extra-intestinal sites by these trophozoites. For diagnosis purposes, the feaces of an infected host are diarrheic and bloody. The trophozoites in feacal material cannot undergo encystations since they are not dehydrated. Consequently, the parasites cannot survive for a long duration since they cannot encyst into a more environmentally resilient form. The infection can be complicated secondary infection by other pathogenic micro-organisms such as bacteria, fungi and viruses. There is need for accurate diagnosis in order to administer effective treatment against the parasite. A definite diagnosis is made after observation of clinical symptoms, presence of ingested red blood cells in the erythrocytes and physical appearance of the cysts and trophozoites. After a given time duration, the mature trophozoites undergo encystation and revert to infective cysts. The cysts at the infective stage are excreted in feces and can be transmitted to another human host via oral ingestion of food and drink contaminated with fecal material containing E. histolytica. High standard hygiene is encouraged as it’s a means of containing Entamoeba histolytica infection (University of Manitoba, 2000).
Entamoeba histolytica strains are differentiated from other strains of pathogenic micro-organisms via observation of physiological characteristics. These entail: growth ability at reduced temperature, base ratio of DNA contents, DNA homology and genome size. It is also dependent on zymodemes, phenotypic patterns of isoenzymes. Identification of zymodemes utilizes phenotypic isoenzymes e.g. malateNADP oxidoreductase(ME), Phosphoglucomutase(PGM), glucose phosphoisomerase(PGM), hexokinase(HK) etc. Depending on these isoenzyme patterns,this parasite can be classified into 22 zymodemes of which 7 represent potentially pathogenic strains (Guptee, 1999).
In respect to Entamoeba histolytica pathogenesis, invasiveness is mainly dependent on the particular zymodeme. It also correlates with collagenase, cytotoxic immunologic proteins, phagocytosis, host’s ability to trigger histolysis and an inflammatory response. Other bacterial, fungal and viral infections can also enhance pathogenicity. Man is the sole reservoir of Entamoeba histolytica infection and the cysts bearing four nuclei are the main infectious agents. This parasite is the causative agent of dysentery which is characterized by bloody and mucoid feaces. There are also systemic complications such as anorexia, nausea and headache. Other rare complications include: severe hemorrhage, colon dilation, stricture formation and amoeboma. The amoebomas mainly affect the caecum and they can easily be confused with carcinoma. The incubation period varies from a few days to several months. Intestinal lesions arise as a result of chronic intestinal amebiasis and acute amebic dysentery. In addition they also cause penis amebic ulcers, amebic vaginitis, and extraintestinal lesions. The latter includes: amebic liver abscess, amebic hepatitis, lung abscess, cerebral abscess, splenic abscess and granulomatous lesions (Guptee, 1999)
Amebic Intestinal Ulcers
The size of intestinal ulcers is about 1 inch diameter with the shape being spherical. The base is broad and the neck is narrow. Its margins are undermined or ragged. Superficial ulcers do not penetrate into the muscularis mucosa whereas deep ulcers extend into the submucous coat. Microscopy study of ulcers reveals a central necrosis area and no amoeba is observed. However towards the periphery, numerous Entameba histolytica trophozoites can be viewed. These ulcers are commonly distributed along the intestine and even in the caecum, rectum and hepatic flexure. Chronic ulcers are superficial, small, and they cause thinning, scarring, succulation, dilation as well as scarring of the intestinal wall. There is also extensive adhesion of adjacent regions and masses that resemble tumors also form.
This mainly entails microscopic examination of fecal material or exudates from the colon which are obtained via sigmoidoscopy. Diagnosis is confirmed upon observation of motile trophozoites that have ingested erythrocytes. However, the presence of E.histolytica cysts does not indicate the presence of disease. Barium enema and sigmoidoscopy examination can also reveal ulceration at the colon but are rarely utilized for diagnosis (Kumar & Clark, 2005).
Amoebic antibody fluorescent tests can be applied and they are positive for over 90% patients showing complications of liver abscess as well as 70% of those suffering from active colitis. Other serological techniques include indirect agglutination, latex agglutination and countercurrent immunoelectrophoresis. Culturing is carried out using Craig’s medium, Balamuth’s medium, lock egg albumin medium and lock egg serum medium. DNA probes allow for specific and rapid diagnosis (Guptee, 1999)
Metronidazole is the medication of choice and 800mg are administered thrice daily for five days in case of amoebic colitis. For liver abscess, a lower dose of 400mg is given in the same time. Other alternative medication that is equally effective includes: chloroquine, dehydroemetine, tinidazole, secnidazole and diloxanide furoate. After treatment, all the parasites need to be cleared from the bowel using a luminal amoebicide like diloxanide furoate (Kumar & Clark, 2005)
Pneumonia-Causes, symptoms, diagnosis and treatment
Pneumonia is a disease that is characterized by lung inflammation and bacteria are the main causative agent. It is mainly manifested as an acute ailment. The common diagnostic symptoms include the presence of a persistent cough, fever and purulent sputum. It is a very potent ailment and the discovery of antibiotics has gone a long way in containing the ailment. However it is still a fatal condition and major cause of mortality of individuals over 70 years. Other diseases also predispose a patient towards contracting pneumonia. HIV is the most common disease and most patients are highly susceptible to bacterial pneumonia (British Thoracic Society, 2002).
The disease can be classified either in terms of aetiology or anatomy. Classification on the basis of anatomy refers to site of infection. The disease can be localized in which case the entire lobe or other lobes are affected. It can also be diffuse and this is infection of the lung’s lobules; usually coupled with the bronchioles and bronchi (bronchopneumonia). Classification by aetiology is on the basis of causative agents which comprise of a variety of bacteria. These include: Mycoplasma, Chlamydia, Coxiella burnetii, Streptococcus pneumonia and Legionella. Other causes include radiotherapy, allergic mechanisms and vomit aspiration (British Thoracic Society, 2002).
Many precipitating factors contribute to pneumonia. Patients suffering from viral infections such as parainfluenza and influenza are highly susceptible to Strep. Pneumoniae. Patients admitted in hospital wards are commonly infected with gram negative bacteria. Tobacco smoking is rated as the highest risk factor for contracting invasive pneumococcal disease. Immunosuppression as a result of AIDS or cytotoxic therapeautic agents can result to pneumonia. The organisms concerned include cytomegalovirus, Mycobacterium avium-intracellulare and Pneumocystis. Other precipitating factors include: inhalation resulting from oesophageal obstruction, Bronchial obstruction arising from carcinoma, bronchietasis and excessive alcohol consumption (Kumar & Clark, 2005).
Causes of Pneumonia
There are different types of pneumonia which arise depending on the causative agent. These include: viral pneumonia, Mycoplasma pneumonia, opportunistic infections, aspiration pneumonia, diffuse pneumonia (bronchopneumonia), cryptogenic organizing pneumonia (COP), rare Causes as well as other causes arising from bacterial infection.
Viral pneumonia is very rare in adults but is mainly as a result of adenovirus or influenza A virus infection. These viral infections predispose patients to pneumonia caused by bacteria. The viruses destroy the epithelium of the respiratory tract thereby enhancing bacterial infection. The most common endemic viral infections include SARS and H5N1.
a. Severe acute respiratory syndrome (SARS)
This is caused by a unique coronavirus with the incubation period lasting for about 5 days. Its mode of transmission is via droplet infection between humans. This infamous outbreak was a health risk in 2003. The symptoms during the first week include headache, malaise, rigors and fever. The symptoms escalated the following week to thrombocytopenia, lymphopenia, diarrhea, breathlessness and a persistent cough (Weinstein, 2004).
b. Influenza A (H5N1)
Normally, humans are not aff3ected by this disease but it has been recently transmitted to humans from fowls thereby overcoming the barrier across species. The symptoms include: cough, breathlessness, diarrhea and cough. The disease progresses to cause lymphopenia and thrombocytopenia. Mortality is very high and mass culling is undertaken to contain the disease.
2. Mycoplasma pneumonia
This is one of the most common pneumonia and occurs after 3-4 years. It mainly affects patients their teenage and early adult years. The disease is more prevalent amongst people whose movement is restricted e.g. boarding facilities and prisons. The main symptoms include malaise and headaches followed by chest problems after 1-5 days. The cough is not conspicuous during the initial stages and chest symptoms are also minimal.
With regard to diagnosis, a chest X-ray is not sufficient. Normally one lobe is affected but in some cases, shadowing might be observed in the two lobes of the lungs. However, there exists no correlation between a patient’s health state and X-ray appearance. The cell count of white blood cells is not raised. Diagnosis s verified by an increasing antibody titre. Treatment is via administration of macrolides e.g. tetracycline and erythromycin. Patients recover after 10-14 days but relapses are known to occur. Worst case scenario results to extrapulmonary complications which can arise any time in the course of the of the ailment. These include: Pericarditis, myocarditis, thrombocytopenia, hemolytic anaemia, erythema multiforme, rashes, arthralgia, meningoencephalitis, neurological abnormalities and gastrointestinal problems such as diarrhea, vomiting etc.
3. Opportunistic Infections
Patients whose immune system is compromised are highly susceptible to developing pneumonia as compared to healthy human hosts. The opportunistic infections include: cytomegalovirus,Cryptococcus, Pneumocystis carinii, Nocardia asteroids, Actinomyces israelii, Karposi’s sarcoma, Mycobacterium avium-intracellulare(MAI) and lymphoid interstitial pneumonia.
Pneumonia and bronchitis arise after cytomegalovirus infection. Over 50% of the population has latent infection but the infection is mainly symptomless.
This fungus infection leads to pulmonary complications comprising of effusions and enlargement of the intrathoracic lymph nodes.
c. Pneumocystis carinii pneumonia(PCP)
This is a very common opportunistic infection leading to pneumonia. It is prevalent in patients suffering from AIDS especially if the CD4 T-lymphocyte count is less than 200 /mm3.The disease is also prevalent in patients undergoing immunosuppressive therapy. P.carnii pneumonia is frequent among malnourished children and it’s also found in the air. Infection is mainly via reinfection as opposed to reactivation of organisms acquired during childhood(British Thoracic Society, 2002).
Symptoms include dry cough, breathlessness and high fever. Tests include radiography and a positive radiographic appearance of PCP comprises of interstitial shadowing at perihilar regions and diffuse bilateral alveolar. Chest X-ray appearances comprise of localized infiltration, cavitation, nodules and pneumothorax. The infiltrates are localized in the upper zones for countries in which HAART is unavailable and for patients taking pentamidine as a form of prophylaxis. A definite diagnosis is obtained via sputum stimulation with saline. Fibreoptic bronchoscopy utilizing bronchoalveolar lavage can also stimulate production of sputum. The diagnosis is subsequently made via sputum staining by utilizing indirect immunofluorescence using monoclonal antibodies (British Thoracic Society, 2001).
d. Nocardia asteroides
The resultant pneumonia is very severe. Test chest X-ray has irregular opacities in one or both lungs especially at the mid zones. Sulfadiazines are the main form of treatment.
e. Actinomyces israelii
This fungus causes severe emphysema, lung abscess and pneumonia. Treatment is via surgical drainage coupled with high–dose penicillin administered intravenously for about 4-6 weeks.
f. Kaposi’s sarcoma
This malignant cancer was peculiarly high in homosexual men infected with HIV. After cutaneous symptoms, the disease progresses to intrathoracic symptoms and these are manifested via nodules, lung infiltrations, endobronchial lesions and enlargement of lymph nodes. There is also a persistent cough and progressive dyspnoea. Chest X-ray is not sufficient as it is not specific. However, bronchoscopy reveals purple/red flat lesions that are recalcitrant biopsy and histological diagnosis. Chemotherapy treatment is via administration of 2 mg vincristine and 10 mg bleomycin every three weeks.
g. Mycobacterium avium-intracellulare (MAI)
This bacterium is the main causative agent for pneumonia for patients suffering from AIDS especially when the CD4 T-lymphocyte count is below 100 mm3. In most cases the pulmonary complications are minimal. The treatment regimen comprises of rifampicin/rifabutin, with clarithromycin, clofazimine and ethambutol. Another regimen comprises of ciprofloxacin with ethambutol and rifabutin.
h. Lymphoid interstitial pneumonia
The disease is rare in adults and highly prevalent in children. It is characterized by immunoblast, plasma cells and lymphocyte infiltration. The causative agent is not yet established and it’s mainly postulated to be a virus. The chest X-ray is distinctly characterized by infiltrates of diffuse reticulonodules. Treatment is via zidovudine or corticosteroid therapy.
4. Aspiration Pneumonia
This arises when gastric contents are aspirated into an individual’s lungs. This can lead to very severe and occasionally fatal ailments as a result of intensive destruction caused by gastric acid. The condition is referred to as Mendelson’s syndrome and is known to complicate anaesthesia especially during delivery. Aspiration also occurs during bulbar palsy, reflux oesophagitis, impaired consciousness (like sleep) especially if the patient does not suffer from trachea-oesophageal fistula. With regard to the anatomy of the bronchi, common spillage sites include the posterior and apical segments at the lower lobe in the right section.
Anaerobes are the main causative agents of persistent pneumonia which normally progresses to bronchieectasis and lung abscess.These anaerobes include: bacterial cocci, fusobacteria and dark-pigmented bacteroids. Early diagnosis averts pulmonary complications and treatment is promptly administered on the patient. Treatment normally targets both aerobic and anaerobic organisms. The regime comprises of1g cefuroxime, 500mg metronidazole for about 5 days. This is followed by metronidazole and oral cofactor for prolonged durations and this depends on bacteria sensitivity.
5. Diffuse Pneumonia (bronchopneumonia)
This is a very common pneumonia. The symptoms are similar to severe bronchitis but can be differentiated by presence of patchy shadows on chest X-ray films and strained bronchial breathing. Diffuse pneumonia is mainly a terminal ailment and affects patients suffering from fatal conditions like cancer. These patients are unable to cough up secretions retained in the lungs and this facilitates widespread lung infection. Aggressive antibacterial therapy is essential and is dependent on the prevailing clinical circumstances.
6. Cryptogenic organizing pneumonia (COP)
The aetiology of this pneumonia is yet to be identified. Patients affected normally present recurrent or single episodes of cough coupled with malaise, fever and breathlessness. In some cases there is persistent chest pain but it is rare for patients to exhibit finger clubbing. Confluent parenchymal shadowing is noted on chest X-ray. Restrictive defects are shown in lung function tests. However the CD4 T-lymphocyte count is normal. A lung biopsy is conclusive as it will show connective tissue buds at the bronchioles and also alveolar ducts. Diagnosis is arrived at on the basis of chest X-ray appearance and patient history. Effective treatment normally comprises of corticosteroid therapy but the disease is known to recur particularly in older women.
7. Other Pneumonia variants
a. Chlamydia Psittaci
This affects individuals upon exposure to birds that are infected especially parrots although infections also occur without this type of contact. The disease incubates for 1-2 weeks and symptoms might arise after several months. The symptoms include: high fever, malaise, muscular pains and cough. There is enlargement of the spleen and liver as well as rose spots around the abdomen. Rarely there are symptoms of a stiff neck, swinging fever and photophobia with dramatic prostration. Diffuse or segmental pneumonia is observed on the chest X-ray. Diagnosis is verified using complement fixing antibody. Treatment is carried out using antibiotics such as tetracycline and macrolides.
b. Staphylococccus aureus
This bacterium does not cause pneumonia but only does so after a viral illness of influenza. This infection begins in the patient’s bronchi and leads to patchy zones of consolidation at the lobes. Full blown infection is characterized by lung abscesses which can be recognized as cysts on chest X-ray. Septicaemia also arises and organs develop metastatic abscesses. Zones of pneumonia i.e. septic infarcts are quite common in cases of staphylococcal septicaemia. This is prevalent amongst patients who use catheters for parenteral infection as well as intravenous drug addicts/abusers. The injection site is normally infected with staphylococcus. Fulminating Pneumonia as a result of staphylococcus infection can cause death within hours. Therefore, intravenous antibiotics should be promptly administered.
c. Chlamydia pneumoniae
This infection mainly spreads from one person to another without the any animal/avian reservoir. The disease is common within institutions and families. 10% of patients presenting community acquired pneumonia are normally infected with C. pneumoniae. 50% of these infections normally result to mild C.pneumoniae(50%), flu(10%), respiratotry tract illness(12%) and acute bronchitis(28%). Immunoflurescence tests that are type specific are required for accurate diagnosis. Effective treatment requires administration of tetracycline and macrolides.
d. Haemophilus influenza
This type of pneumonia is known to cause exacerbation amongst chronic bronchitis and COPD patients. The pneumonia is either confined to single lobe or diffuse. However are no distinct features to distinguish it from other pneumonias caused by bacteria. Treatment is via oral administration of amoxicillin (4 × 500mg) daily.
e. Legionella pneumophila
There are 3 epidemiological patterns of the disease. First, it is exhibited in form of outbreaks amongst healthy individuals residing in institutions, hotels and hospitals in which case cooling systems and shower facilities are contaminated. Secondly, it arises in sporadic cases and the cause of infection is not identified. Third, there are outbreaks in patients whose immune system is compromised.
This bacterium proliferates even at temperatures of 40°C and it’s an airborne disease. Temperature control and adequate treatment of water can effectively limit infection. Incubation takes 2-10 days and the rate of male infection is twice that of females. Infection is usually mild but occasionally, there is occurrence of fever, myalgia, headache and malaise. Over 50% of patients have diarrhea, vomiting, abdominal pains, nausea and gastrointestinal complications. Some patients exhibit mental confusion, neurological signs, haematuria, renal failure and acute illness. Initially a patient has a dry cough that may later become purulent. Chest X-ray films reveal lobar and later multilobar shadowing with pleural effusion. A presumptive diagnosis is made if the following four features are observed in the patient. These comprise of: hyponatraemia, prodromal illness that is viral-like, lymphopenia and a dry cough, confusion or diarrhea. Other diagnostic symptoms include high levels of aminotransferases in the liver and serum as well as hypoalbuminaemia.
Confirmatory diagnosis is made via direct immunofluorescent staining of bronchial washings, sputum or pleural fluid. Culturing is also undertaken on special media and this takes 3 weeks. However gram staining is not applicable. Commercial urinary, antigen tests can be used. Treatment requires administration of macrolides and clarithromycin is commonly used. Rifampicin and ciprofloxacin are also used. mOst patients make a full recovery but mortality occurs in 30% of elderly patients.
f. Coxiella burnetii
The symptoms of this pneumonia comprise of headache, malaise and fever. Chest X-ray films have multiple lesions. The pneumonia is chronic and is often linked to endocarditis. Diagnosis is confirmed by a high titre of complement-fixing antibody. Treatment is via administration of tetracycline or macrolides. Rifampicin is prescribed for severe cases.
g. Gram-negative bacteria
A variety of gram-negative bacteria cause pneumonia and infections are normally nosocomial in nature.
i. Moraxella catarrhalis
The pneumonia caused by this bacterium is linked to fatal pneumonia and COPD exacerbations. Some bacterial strains are potent and resistant to amoxicillin as they secrete β-lactamase. The organism is also linked to bronchopulmonary infection.
ii. Pseudomonas aeruginosa
This bacterium is the causative agent of cystic fibrosis and pneumonia is observed in these patients. Pneumonia also affects neutropenia patients especially after cytotoxic chemotherapy. Treatment involves antibiotic administration of ciprofloxacin (400mg i.v. for 50 minutes twice daily), ticarcillin (15g daily i.v. infusion) or ceftazidime( 2g bolus i.v. 8-hourly). Piperacillin is also effective against the bacteria. These penicillins should be administered with an aminoglycoside such as netilmicin or gentamicin. Blood levels need to be monitored since aminoglycosides are ototoxic and nephrotoxic (Lim, 2004).
iii. Klebsiella pneumoniae
This pneumonia normally affects elderly individuals especially those who consume excess alcohol or have has a history of malignancy, diabetes, lung or heart disease. The initial onset is rather sudden and characterized by severe systemic complications. The patient’s sputum is blood-stained, gelatinous or purulent. This pneumonia infection affects the upper lobes and consolidation is usually extensive. The infected lobe also swells and this is exhibited as fissure bulging on chest X-ray films. Klebsiella is found in both the blood and sputum. Treatment is via administration of a cephalosporin although this is dependent on the organism’s sensitivity. Mortality is reported to be high especially if there is a predisposing illness (Kumar & Clark, 2005).
h. Anaerobic Bacteria
The pneumonia infections arise in individuals suffering from other diseases like diabetes and it’s also linked to aspiration. In case of bacteroides, treatment is via administration of metronidazole. Generally, prognosis is dependent on the causative organism and precipitating cause.
Common Pneumonia complications
Lung abscess and emphysema are common complications of pneumonia. The former is characterized by severe lung suppuration. Chest X-ray films show cavity formation. Bronchial obstruction or carcinoma results to lung abscess. The abscesses also arise from specific pneumonias due to infection by Klebsiella pneumoniae or Staphylococcus aureus. Septic embolidue to staphylococci infection leads to multiple lung abscesses. Empysema refers to the presence of pus in the pleural cavity. It commonly results from severe pneumonia and even lung abscess rupture. Anaerobic organisms normally proliferate in the pleural cavity and the patients are severely ill. They exhibit neutrophil granulocytosis and high fever (Lim, 2004).
General Diagnosis and Treatment of Pneumonia
Preliminary pneumonia testing normally comprises of blood and sputum examination. Patients with severe pneumonia should be hospitalized and chest X-ray films are routinely taken. Investigations on blood gases aid in the detection of respiratory failure. Different types of pneumonia are diagnosed via specific testing. Pneumococcal antigens are detected via counter-immunoelectrophoresis of serum, urine or sputum. Legionella antigen is detected via urine analysis. Chlamydia and Legionella antibodies are detected via immunofluorescent tests. IgM and IgG mycoplasma antibodies are detected in convalescent and acute samples.
Empirical therapy is largely prescribed for Streptococcus pneumoniae infections. Mycoplasma infections are also responsible for a significant number of pneumonia infections. Antibiotic resistance has posed a major stumbling block to bacterial infections. However there is no evidence that links new antibiotics to a therapeutic advantage. Consequently, amoxicillin is the medication of choice for treatment of community acquired pneumonia. It is normally administered orally at 500mg doses after every 8 hours. For patients sensitive to penicillin, clarithromycin or erythromycin can be orally administered. Severe pneumonia cases require a treatment regimen that comprises of a macrolide(clarithromycin/erythromycin) and amoxicillin. Parenteral benzylpenicillin or ampicillin is given in combination with clarithromycin (Kumar & Clark, 2005).
Upon confirmation of Staphylococcus aureus, flucloxacillin in combination with sodium fusidate should be administered on the patient. For patients allergic to macrolides or penicillin, fluoroquinolones are highly recommended. Severe pneumonia patients require parenteral antibiotics prescribed together with broad spectrum and lactamase tolerant beta-lactam antibiotics. An example of such a therapeutic regimen comprises of (cefuroxime/co-amoxiclav) and clarithromycin. The parenteral antibiotics should immediately change to oral especially if the temperature stabilizes for 24 hours. Generally treatment is specific after confirmatory, microbiological results. However, a health practitioner needs to realize that in 10% of pneumonia cases, mixed infections are normally the cause. Only 5% of patients suffering from community acquired pneumonia are admitted to hospital. However over 25% of patients suffering from pneumonia as a result of Staphylococcus aureus are admitted to hospital. Mortality is normally attributed to lack of sufficient or appropriate medication during the initial infection stages.
Nosocomial pneumonias need to be closely monitored inorder to check on other possible causes such as pulmonary embolism, heart/lung failure etc. Mild nosocomial pneumonia require administration of coamoxiclav but severe cases need a very aggressive therapeutic regimen of antibiotics. Infections of gram negative bacteria are very common for nosocomial pneumonias and treatment is via cephalosporins such as cefuroxime in combination with aminoglycosides such as gentamicin. Patients suffering from chronic chest infections and those in which Pseudomonas infection is likely need intravenous ceftazidime or ciprofloxacin. Immunosuppressed patients should be prescribed for broad-spectrum antibiotics, antiviral and antifungal agents. Nosocomial aspiration pneumonia is relatively common and mainly arises as a result of multiple bacterial infections especially anaerobes. Oral administration of medication is highly inappropriate for this group of patients. A recommended therapeutic regime comprises of rectal or intravenous metronidazole and cefuroxime or co-amoxiclav.