1.1 Definition of Leptospirosis
Leptospirosis is an example of zoonotic disease (spread from animals to humans) for which globalization and social variation have different epidemiological patterns for the poor and rich community. According to the Malaysia Ministry of Health (KKM) official website, the other names for this disease are Weil’s disease, Icterohemorrhagic fever, Swineherd’s disease, Rice-field fever, Cane-cutter fever, Swamp fever, and others. This disease is a significant health problem in developing countries especially for the poor rural society (Bharti, 2003). It has been reported that this disease commonly occurs in tropical and subtropical countries that are suitable for the bacteria's growth and it can reach more than 1 million cases per year globally. Malaysia is one of the Southeast Asia countries that has a significant increase in disease outbreaks and reported cases in recent years (Garba, Bahaman, Khairani-Bejo, Zakaria, & Mutalib, 2017). Until now, Malaysia is endemic for Leptospirosis with increasing cases recorded over the years.
Leptospira Bacteria is a photograph by Kateryna Kon/science Photo Library which was uploaded on October 1st, 2018.
Electronic image of Leptospira interorgans
Leptospirosis disease is caused by the spirochetes bacteria belonging to the genus Leptospira. These bacteria are gram-negative and aerobic bacteria. The common size of bacteria is 20 micrometers long and it has a right-handed helical (Karpagam & Ganesh, 2020). Sixty-six different species of Leptospira have been discovered and it has been divided into 2 clades and 4 subclades (P1, P2, S1, S2) according to their genomic sequence. 8 of 19 species from the P1 (L. borgpetersenii, L. alexanderi, L. interrogans, L. mayottensis, L. kirschneri, L. noguchii, L. weilii, & L. santarosai) can cause severe disease and 21 species from P2 were believed could cause mild disease in human. Other 26 species belong to the S1 and S2. They are saprophytes that undergo saprotrophic nutrition (Caimi & Ruybal, 2020). Rodents, cattle, dogs, horses, sheep, swine and wild animals are believed to be the reservoir hosts of the bacteria (Ellis, 2015).
1.2 History of Leptospirosis in Malaysia
In April 1925, Fletcher encountered by chance the first case of leptospirosis in the Institute of Medical Research, Kuala Lumpur, Malaysia 10 years after the isolation of Leptospira for the first time from human patient blood in Japan (Inada, Ido, Hoki, Kaneko, & Ito, 1916). Fletcher also identified 3 different serovars (Leptospira interrogans serovar Icterohaemorrhagiae, Hebdomadis, and Pyrogenes) after isolating the pathogen from the liver, blood and kidney from the 21 patients in Malaysia. The blood from a patient with unknown origin fever was inoculated into guinea pigs and it developed jaundice and hemorrhages in the nose. The guinea pig died 13 days after inoculation and the postmortem result showed signs of leptospirosis. Fletcher also introduced a new medium in semi-solid form that is widely used in many laboratories nowadays for the isolation and maintenance of the leptospira culture (Fletcher, 1928).
Picture of two cultures of Leptospira sp. strain Manara. Two cultures of Leptospira sp. strain Manara in Fletcher medium supplemented with 3% (left tube) and 1% (right tube) seawater after 48 h of incubation at 28°C. The dinger rings corresponding to Leptospira sp. growth is indicated with red arrows. doi:10.1371/journal.pone.0144974.g001
In the earlier stage of work regarding the Leptospirosis in Malaysia, it only focused on the patients who were in the military hospital. In 1957, it was reported that 614 military personnel and 238 civilian patients admitted at the military hospital were suffering from the fever. Based on the serology test, 34.7% and 13% respectively were confirmed to have Leptospirosis (McCrumb et al, 1957). There was also a previous study that concluded that rubber plantation laborers and the workers at sewage, drainage, forestry, and town cleaning as well as antimalarial workers were exposed to high risk of Leptospirosis infection and become the an occupational disease (Shafie et al, 2012). However, travel to endemic areas and recreational activities such as water sports have increasingly been reported as a major risk for this infection (Victoriano et al, 2009).
In 2014, it was reported that the peak of the leptospirosis cases was 7806 confirmed cases with 92 deaths (Zainudin, 2015). It does not include the cases that may be under-reported or misdiagnosed and it can be considered as a significant public health threat locally. In 2016, it has been reported that forty-two patients with confirmed diagnosis of leptospirosis in Perak. The case fatality rate was 14.3%. Malay ethenic was the most affected by the diseases and majority of them were male (Fann, Vidya, Chong, Indralingam, & Christoper Chan, 2020). Minly, the outbreak would occur after the effect of heavy rainfall or flood season and it can be a seasonal incidence.
1.3 Transmission of The Disease
Leptospirosis is transmitted by pathogenic or saprophytic Leptospires (World Health Organization, 2003). Pathogenic and saprophytic leptospires can both be found in the renal tubules of animals that are hosts, while saprophytic leptospires are more common in damp or tropical climates. Saprophytic leptospires species contaminate waterways without necessitating a host, thrive only on organic matter, and do not infect humans (The Leptospirosis Information Center, 2010). Pathogenic Leptospires, on the other hand, require a host to reproduce (Institute for International Cooperation in Animal Biologics, Center for Food Security and Public Health. Leptospirosis, 2005). Pathogens can be transmitted into the ecology through the urine of animals carrying pathogenic Leptospirosis. The rodent hosts that contain this pathogenic leptospire suffer no harm. They are often described to as "natural hosts."
In a polluted environment, leptospirosis can be spread directly or indirectly from one host to another. When an animal's excrement is expelled, it pollutes the soil and water. After consuming contaminated water, humans are impacted. The dangerous Leptospira bacteria can potentially be passed on to people through contaminated food. By coming into direct touch with Leptospires through wound infections, food, and drink, the individual can be infected. When exposed to dirty water for an extended period of time, it can enter the human body through the nasal, oral, and ocular mucosa. After penetrating the In the 2000 Eco-Challenge multisport race in Malaysian Borneo, a large number of competitors experienced leptospirosis. The Centers for Disease Control and Prevention interviewed 189 people, and 80 (42%) of them fulfilled the leptospirosis clinical diagnosis. Exposure to the rain-swollen Segama river for long periods of time was one of the risk factors (photograph (a) credit Reed Hoffmann). Whereas in B section, it is portrayed there was a small community in an area that is a typical leptospirosis epidemiologic environment. Citizens of tropical regions with significant rainfall are more likely to contract leptospirosis, especially if residual water is contaminated with excrement from wild or domesticated animals, which can operate as intermediate hosts for pathogenic Leptospira species.
Leptospirosis can also disseminate through the airways. When Leptospires in urine dissipate into air droplets and are inhaled by individuals, they can lead to disease. Even though human-to-human disease transmission is unusual, it should be recognised that consensual sex and nursing could allow pathogenic Leptospires to passed from one generation to another (Lim, 2010). In addition, an infected woman's unborn child may be exposed to hazardous Leptospires. Individuals can expel leptospires in their urine for up to eleven months. Rodents and wild animals such as cattle, pigs, rats, buffaloes, and dogs, which develop leptospires in their urinary tract for months or years, are a reservoir of pathogenic Leptospires. The predominant carriers of pathogenic Leptospires would be all these animals.
Leptospira may persist in the environment for long periods of time because of the significant dampness and moderate temperatures. In particular, strong rains and numerous floods, especially during the monsoon season, intensify the leptospirosis outbreak. Leptospirosis, on the other hand, has a seasonal distribution, with the bulk of reported cases during the rainy season and following floods (Benacer, 2016). The majority of cases are caused by occupational exposures and recreational activities. Veterinarians, zookeepers, pet store owners, butchers, and other professionals who work with wild animals on a daily basis are more vulnerable. Military personnel, farmers, fishers, and plumbers, for instance, engage in situations that include water, mud, and sludge, and are thus particularly vulnerable to the human body, leptospires invade the circulatory system and attack bodily tissues and organs.
1.4 Stage Level and Symptoms of the Disease
Leptospirosis is divided into two categories. First category is known as mild leptospirosis, which is the most common type of leptospirosis, accounting for 90% of cases. Muscle soreness, chills, and even a headache are some of these symptoms. Second is extensive leptospirosis which can develop in between 5% and 15% of cases. If the bacterium affects the liver, kidneys, or other vital structures, it can cause organ damage, internal hemorrhaging, and fatality.
Leptospirosis usually takes 5-14 days to develop, although it can span anything else from 2 to 30 days. In contrast, a patient does not display clinical symptoms in less than 24 hours except if the volume of germs penetrating the body is bigger than normal. In most cases, the infection is systemic and affects the entire body. Anicteric leptospirosis and icteric leptospirosis are the two forms of infection that present with diverse clinical manifestations (Madhu & Aparna, 2008).
Anicteric leptospirosis is a type of leptospirosis that does not induce jaundice in 90% of cases (Lim et al., n.d.). Anicteric leptospirosis patients go through phases 1 and 2 of the illness. The sickness is invariably associated with aseptic meningitis in the anicteric subtype of leptospirosis (Madhu & Aparna, 2008). A less severe form of leptospirosis is rarely lethal, but it can trigger pulmonary bleeding and mortality even if there is no jaundice. Flu-like characteristics such as severe headaches, rapid fevers of 39°C or higher, eyes inflammatory, muscle aches, diarrhea, lethargy, nausea and vomiting, chills, rigors, and maculopapular rashes are present in phase 1, also known as acute or septicemic phase.
Anti-leptospira antibodies proliferate during phase 2 (the immunological phase), allowing leptospirosis pathogens to be discovered in the patient's urine output. Infected individuals become ill again during this phase, which can last up to 30 days or longer (Leptospirosis Information, 2021). Some people, however, do not progress to the second stage of the illness. The remaining 10% of patients progress to icteric leptospirosis, often known as Weil's syndrome (Lim et al., n.d.). The second phase of anicteric leptospirosis is far more severe than the first. The bulk of the clinical manifestations are identical to anicteric leptospirosis, however the sickness can progress to be lethal. Within 10 days, organs such as the liver, kidneys, brain, heart, and central nervous system are affected.
Leptospirosis in its clinical phase was observed in figure above. At section A, a 37-year-old man who raised pet rats developed subconjunctival hemorrhages and icterus, as well as fever, myalgia, and severe headache. He had impaired liver and kidney functionality when he was hospitalized. One week after manifestation, serological tests for leptospiral antibodies shifted from negative to positive. He was given injectable penicillin and made a full recovery (Haake & Levett, 2014). Whereas at section B, it's reported that A 50-year-old guy experienced a devastating lung hemorrhage after returning from a trip in Malaysia, where he had wandered through mangrove woods. On the second day of admission, the patient's respiratory condition deteriorated, necessitating mechanical respiration and a blood transfusion. He was given doxycycline first, then amoxicillin, and he recovered slowly yet entirely. Four months following injection.
No comments:
Post a Comment