FInal Laboratory activity Microbiology

Jan Elmer L. Labesores May 7, 2021

BSN-1B

Discuss each stages of the parasites (from cyst or eggs-larvae- adult forms)
LIFE CYCLE OF ENTAMOEBA HISTOLYTICA

Cysts and trophozoites are passed in feces (1). Cysts are typically found in formed stool,
whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica
occurs by ingestion of mature cysts (2) in fecally contaminated food, water, or hands.
Excystation (3) occurs in the small intestine and trophozoites (4) are released, which migrate to
the large intestine. The trophozoites multiply by binary fission and produce cysts (5), and both
stages are passed in the feces (1). Because of the protection conferred by their walls, the cysts
can survive days to weeks in the external environment and are responsible for transmission.
Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested
would not survive exposure to the gastric environment. In many cases, the trophozoites remain
confined to the intestinal lumen (A: noninvasive infection) of individuals who are asymptomatic
carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal
mucosa (B: intestinal disease), or, through the bloodstream, extraintestinal sites such as the
liver, brain, and lungs (C: extraintestinal disease), with resultant pathologic manifestations. It
has been established that the invasive and noninvasive forms represent two separate species,
respectively E. histolytica and E. dispar. These two species are morphologically
indistinguishable unless E. histolytica is observed with ingested red blood cells
(erythrophagocystosis). Transmission can also occur through exposure to fecal matter during
sexual contact (in which case not only cysts, but also trophozoites could prove infective).
LIFE CYCLE OF HIV

Binding and Fusion: HIV begins its life cycle when it binds to a CD4 receptor and one of two co-
receptors on the surface of a CD4+ Tlymphocyte. The virus then fuses with the host cell. After
fusion, the virus releases RNA, its genetic material, into the host cell. Reverse Transcription: An
HIV enzyme called reverse transcriptase converts the singlestranded HIV RNA to double-
stranded HIV DNA. Integration: The newly formed HIV DNA enters the host cell's nucleus,
where an HIV enzyme called integrase "hides" the HIV DNA within the host cell's own DNA. The
integrated HIV DNA is called provirus. The provirus may remain inactive for several years,
producing few or no new copies of HIV. Transcription: When the host cell receives a signal to
become active, the provirus uses a host enzyme called RNA polymerase to create copies of the
HIV genomic material, as well as shorter strands of RNA called messenger RNA (mRNA). The
mRNA is used as a blueprint to make long chains of HIV proteins. Assembly: An HIV enzyme
called protease cuts the long chains of HIV proteins into smaller individual proteins. As the
smaller HIV proteins come together with copies of HIV's RNA genetic material, a new virus
particle is assembled. Budding: The newly assembled virus pushes out ("buds") from the host
cell. During budding, the new virus steals part of the cell's outer envelope. This envelope, which
acts as a covering, is studded with protein/sugar combinations called HIV glycoproteins. These
HIV glycoproteins are necessary for the virus to bind CD4 and coreceptors. The new copies of
HIV can now move on to infect other cells.
LIFE CYCLE OF TAENIA SOLIUM

This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier
image . These eggs are immediately infectious and do not require a developmental period
outside the host. Pigs and humans become infected by ingesting eggs or gravid proglottids
image , image . Humans are usually exposed to eggs by ingestion of food/water contaminated
with feces containing these eggs or proglottids or by person-to-person spread. Tapeworm
carriers can also infect themselves through fecal-oral transmission (e.g. caused by poor hand
hygiene). Once eggs or proglottids are ingested, oncospheres hatch in the intestine image ,
image invade the intestinal wall, enter the bloodstream, and migrate to multiple tissues and
organs where they mature into cysticerci over 60–70 days image , image . Some cysticerci will
migrate to the central nervous system, causing serious sequellae (neurocysticercosis).

This differs from taeniasis, which is an intestinal infection with the adult tapeworm. Humans
acquire intestinal infections with T. solium after eating undercooked pork containing cysticerci
image . Cysts evaginate and attach to the small intestine by their scolices. Adult tapeworms
develop to maturity and may reside in the small intestine for years image .
LIFE CYCLE OF ASCARIS LUMBRICOIDES

Adult worms image live in the lumen of the small intestine. A female may produce approximately
200,000 eggs per day, which are passed with the feces image . Unfertilized eggs may be
ingested but are not infective. Larvae develop to infectivity within fertile eggs after 18 days to
several weeks image , depending on the environmental conditions (optimum: moist, warm,
shaded soil). After infective eggs are swallowed image , the larvae hatch image , invade the
intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs image .
The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the
bronchial tree to the throat, and are swallowed image . Upon reaching the small intestine, they
develop into adult worms. Between 2 and 3 months are required from ingestion of the infective
eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.
LIFE CYCLE OF SCHISTOSOMES

Schistosoma eggs are eliminated with feces or urine, depending on species image . Under
appropriate conditions the eggs hatch and release miracidia image , which swim and penetrate
specific snail intermediate hosts image . The stages in the snail include two generations of
sporocysts image and the production of cercariae image . Upon release from the snail, the
infective cercariae swim, penetrate the skin of the human host image , and shed their forked
tails, becoming schistosomulae image . The schistosomulae migrate via venous circulation to
lungs, then to the heart, and then develop in the liver, exiting the liver via the portal vein system
when mature, image image . Male and female adult worms copulate and reside in the
mesenteric venules, the location of which varies by species (with some exceptions) image . For
instance, S. japonicum is more frequently found in the superior mesenteric veins draining the
small intestine image , and S. mansoni occurs more often in the inferior mesenteric veins
draining the large intestine image . However, both species can occupy either location and are
capable of moving between sites. S. intercalatum and S. guineensis also inhabit the inferior
mesenteric plexus but lower in the bowel than S. mansoni. S. haematobium most often
inhabitsin the vesicular and pelvic venous plexus of the bladder image , but it can also be found
in the rectal venules. The females (size ranges from 7–28 mm, depending on species) deposit
eggs in the small venules of the portal and perivesical systems. The eggs are moved
progressively toward the lumen of the intestine (S. mansoni,S. japonicum, S. mekongi, S.
intercalatum/guineensis) and of the bladder and ureters (S. haematobium), and are eliminated
with feces or urine, respectively
LIFE CYCLE OF HOOKWORM

Eggs are passed in the stool image , and under favorable conditions (moisture, warmth, shade),
larvae hatch in 1 to 2 days and become free-living in contaminated soil. These released
rhabditiform larvae grow in the feces and/or the soil image , and after 5 to 10 days (and two
molts) they become filariform (third-stage) larvae that are infective image . These infective
larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with the
human host, typically bare feet, the larvae penetrate the skin and are carried through the blood
vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend
the bronchial tree to the pharynx, and are swallowed image . The larvae reach the jejunum of
the small intestine, where they reside and mature into adults. Adult worms live in the lumen of
the small intestine, typically the distal jejunum, where they attach to the intestinal wall with
resultant blood loss by the host image . Most adult worms are eliminated in 1 to 2 years, but the
longevity may reach several years.

Some A. duodenale larvae, following penetration of the host skin, can become dormant
(hypobiosis in the intestine or muscle). These larvae are capable of re-activating and
establishing patent, intestinal infections. In addition, infection by A. duodenale may probably
also occur by the oral and the transmammary route. A. ceylanicum and A. caninum infections
may also be acquired by oral ingestion. A. caninum-associated eosinophilic enteritis is believed
to result following oral ingestion of larvae, not percutaneous infection. N. americanus does not
appear to be infective via the oral or transmammary route.
LIFE CYCLE OF BACILLUS ANTHRACIS

When B. anthracis, in the vegetative form, enters the environment, leaving a dying host
organism, sporulation occurs. Dormant endospores are the infectious particle of B. anthracis;
infection only takes place when an endospore enters the body from the environment, whether
through an abrasion on the skin of an organism, through ingestion, or through inhalation. Spores
are ideal infections particles because, as mentioned earlier, they are extremely resistant to
adverse environmental conditions. There have not been any observed cases of transmission of
the disease between two living animals in the wild, because this would require the transfer of
vegetative bacterial cells, not spores.

When B. anthracis spores enter a host organism, they are phagocytosed by regional
macrophages and transported to the lymph nodes (Rao 2010). There, receptors on the inner
membrane of the spore bind to molecules called germinants, which begins the germination
process. The binding of the receptors causes rehydration of the spore and disintegration of the
cortex and the coat (Driks 2009), leaving the vegetative form of B. anthracis. Infection of the
host organism proceeds until it is treated or the host dies, releasing the cells into the
environment and starting the process over.

LIFE CYCLE OF PLASMODIUM

The life cycle of Plasmodium can be divided into two distinct phases: the asexual cycle in
humans and the sexual cycle in mosquitoes. To begin the asexual cycle in humans, an infected
female Anopheles mosquito injects sporozoites into the new human host during a blood meal.
Sporozoites injected into the bloodstream leave the blood vascular system within 30 to 40
minutes and enter the liver. This begins the exo-erythrocytic stage of the life cycle during which
asexual multiplication occurs. Within hepatocytes the sporozoites undergo many nuclear
divisions to become schizonts. This occurs over a period of 6 to 15 days, after which the
schizonts burst and release thousands of merozoites into the circulation (1). This marks the end
of the exo-erythrocytic cycle.

Upon release, the merozoites invade the red blood cells where they undergo another asexual
cycle called erythrocytic schizogony. This is also known as the erythrocytic cycle. During this
stage the merozoites develop to form immature or ring stage trophozoites which then progress
to mature trophozoites. The mature trophozoites develop into schizonts. The erythrocytic cycle
results in the formation of 4 to 36 new parasites in each infected cell within a 44 to 72 hour
period (2). At the end of the cycle, the infected red blood cells burst, releasing the merozoites.
At this stage, merozoites can either infect new red blood cells to begin the erythrocytic cycle
again, or, through the action of some unknown factor, the merozoites can develop into
gametocytes. It is of note that blood stage parasites are responsible for the clinical symptoms of
malaria (1). For example, lysis of the red blood cells is an important cause of malaria-associated
anemia. In addition, if a significant number of infected cells rupture simultaneously, the resulting
material in the bloodstream is thought to induce a malarial paroxysm (2).

Next begins the sexual cycle in mosquitoes. When a female Anopheles mosquito takes a blood
meal from an infected person, both male (microgametocytes) and female (macrogametocytes)
may be ingested. The microgametocytes and macrogametocytes mature to become
microgametes and macrogametes, respectively. In the midgut of the mosquito, the
microgametes fertilize the macrogametes, forming a zygote. The zygote becomes elongated
and motile, and is then called an ookinete. The ookinetes invade the midgut wall of the mosquito
where they develop into oocytes. The oocytes grow and develop and finally rupture to release
sporozoites. The sporozoites make their way to the salivary glands of the mosquito so that they
can be inoculated in to the new human host during the mosquito’s next blood meal, thus
perpetuating the Plasmodium life cycle.

LIFE CYCLE OF ENTEROBIUS VERMICULARIS

Gravid adult female Enterobius vermicularis deposit eggs on perianal folds image . Infection
occurs via self-inoculation (transferring eggs to the mouth with hands that have scratched the
perianal area) or through exposure to eggs in the environment (e.g. contaminated surfaces,
clothes, bed linens, etc.) image . Following ingestion of infective eggs, the larvae hatch in the
small intestine image and the adults establish themselves in the colon, usually in the cecum
image . The time interval from ingestion of infective eggs to oviposition by the adult females is
about one month. At full maturity adult females measure 8 to 13 mm, and adult males 2 to 5
mm; the adult life span is about two months. Gravid females migrate nocturnally outside the
anus and oviposit while crawling on the skin of the perianal area image . The larvae contained
inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions
image .

Rarely, eggs may become airborne and be inhaled and swallowed. Retroinfection, or the
migration of newly hatched larvae from the anal skin back into the rectum, may occur but the
frequency with which this happens is unknown.