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\begin{document}

\title{Two decades of tuberculosis surveillance reveal disease spread, high
levels of exposure and mortality, and marked variation in disease
progression in wild meerkats}



\author[1]{Nadine Müller-Klein}%
\author[1]{Alice  Risely}%
\author[1]{Dominik Schmid}%
\author[2]{Marta Manser}%
\author[3]{Tim Clutton-Brock}%
\author[1]{Simone Sommer}%
\affil[1]{Universitat Ulm Fachbereich Biologie}%
\affil[2]{Universitat Zurich Institut fur Evolutionsbiologie und Umweltwissenschaften}%
\affil[3]{University of Pretoria Mammal Research Institute}%


\vspace{-1em}



  
  \date{May 18, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Infections with Tuberculosis (TB)-causing agents of the
\emph{Mycobacterium tuberculosis} complex threaten human, livestock, and
wildlife health globally due to the high capacity to cross trans-species
boundaries. Tuberculosis is a cryptic disease characterized by
prolonged, sometimes lifelong subclinical infections, complicating
disease monitoring. Consequently, our understanding of infection risk,
disease progression, and mortality across species affected by TB remains
limited. The TB agent \emph{Mycobacterium suricattae} was first recorded
in the late 1990s in a wild population of meerkats inhabiting the
Kalahari in South Africa and has since spread considerably, becoming a
common cause of meerkat mortality. This offers an opportunity to
document the epidemiology of naturally spreading TB in a wild
population. Here, we synthesize more than 25 years-worth of TB reporting
and social interaction data across 3,420 individuals to track disease
spread, and quantify rates of TB social exposure, progression, and
mortality. We found that most meerkats had been exposed to the pathogen
within eight years of first detection in the study area, with exposure
reaching up to 95\% of the population. Approximately one quarter of
exposed individuals progressed to clinical TB stages, followed by
physical deterioration and death within a few months. Since emergence,
11.6\% of deaths were attributed to TB, although the true toll of
TB-related mortality is likely higher. Lastly, we observed marked
variation in disease progression among individuals, suggesting
inter-individual differences in both TB susceptibility and resistance.
Our results highlight that TB prevalence and mortality could be higher
than previously reported, particularly in species or populations with
complex social group dynamics. Long-term studies, such as the present
one, allow us to assess temporal variation in disease prevalence and
progression and quantify exposure, which is rarely measured in wildlife.
Long-term studies are highly valuable tools to explore disease emergence
and ecology, and study host-pathogen co-evolutionary dynamics in
general, and its impact on social mammals.%
\end{abstract}%



\sloppy


\textbf{Introduction}

Pathogens, particularly those causing emerging diseases, can be a major
driver of mortality in wildlife (McCallum, 2008; Fereidouni et al.,
2019; Fisher and Garner, 2020), which can be aggravated by changing
environments and climate change (Dwyer et al., 2020; Paniw et al.,
2022). Cross-sectional studies are often employed to study patterns of
pathogen prevalence and transmission, yet their power to assess
long-term patterns of pathogen emergence, dynamics and overall pathogen
prevalence are limited (Reis et al., 2021). The advantage of
longitudinal surveillance studies rest in their ability to identify
factors underpinning pathogen transmission, assess the impact of
pathogens on individual hosts and populations, and track host-pathogen
dynamics (Ryser-Degiorgis, 2013; Walton et al., 2016; Watsa and Wildlife
Disease Surveillance Focus Group, 2020). Since long-term projects are
difficult to sustain and pathogen monitoring and detection can be
challenging (reviewed in Thomas et al., 2021), such long-term datasets
populations are still exceptional in natural (Patterson et al., 2017;
McDonald et al., 2018).

Pathogens of the \emph{Mycobacterium tuberculosis} complex (MTC), the
causative agents of the disease tuberculosis (TB), are among the most
significant emerging pathogens globally (CSFPH, 2019). Generally\emph{,
Mycobacterium} infections are chronic, progressive and characterized by
prolonged latent (i.e. non-infectious) or subclinical (i.e. without
clinical signs but potentially still infectious to others) periods
(Houben and Dodd, 2016; CSFPH, 2019; Dwyer et al., 2020; Jolma et al.,
2021). If the disease progresses to the development of overt clinical
signs, their onset is usually followed by health decline and death
(Alexander et al., 2010; Fairbanks et al., 2015). A wide variety of
mammals can be infected with MTC bacteria ( CSFPH, 2019; Reis et al.,
2021), which can easily be transmitted between multiple hosts species,
with implications for entire ecosystems (Michel et al., 2006; Hardstaff
et al., 2014). Thus, a well-founded understanding of transmission and
host-pathogen dynamics is imperative for the development of adequate TB
surveillance and management strategies (de Lisle et al., 2002). However,
despite intense research efforts in several TB host systems (reviewed in
Reis et al., 2021), quantitative data TB exposure, prevalence and
progression are still rare for many wildlife species affected by TB.

Meerkats (\emph{Suricata suricatta} ) are highly social, cooperatively
breeding small carnivores (Clutton-Brock and Manser, 2016) native to
southern Africa, a hotspot region for TB in wildlife (Michel et al.,
2006; Tanner et al., 2015). Within the Kalahari Meerkat Project (KMP;
Clutton-Brock and Manser, 2016), a natural population has been routinely
monitored since 1993. First evidence of infections
with\emph{Mycobacterium suricattae} , previously believed to be \emph{M.
bovis} , were reported in the late 1990s (Drewe, Foote et al., 2009;
Parsons et al., 2013). Meerkats have a complex social system
characterized by small to medium sized social groups (two to fifty
individuals). Reproduction is largely monopolized by dominant breeding
pairs (Clutton-Brock and Manser, 2016), which differ from subordinates
in physiology (Young et al., 2006; Smyth et al., 2018), social network
position(Drewe, 2010), and mortality risk (Cram et al., 2018). Social
interactions within and between group are frequent (Clutton-Brock and
Manser, 2016), making meerkats an excellent model to investigate
pathogen transmission in a social context (Drewe, 2010).

Meerkats are a particularly good model system to investigate TB
epidemiology because transmission, progression, and pathology of\emph{M.
suricattae} infection mirrors patterns found in other wildlife hosts:
Transmission occurs mostly via aerial routes or social interactions
(Gallagher and Clifton-Hadley, 2000; Drewe, 2010; Drewe et al., 2011).
Infection are initially characterized by long latent or subclinical
periods (Drewe et al., 2011; Tomlinson et al., 2013; McDonald et al.,
2018), followed by rapid progression to terminal stages upon onset of
clinical signs (Alexander et al., 2010; Fairbanks et al., 2015). Typical
signs of TB infections, including lymphadenopathy, particularly of
submandibular, inguinal and cervical lymph nodes, and physical
deterioration 1990s (Drewe, Foote et al., 2009; Parsons et al., 2013).,
typically develop \textasciitilde{}12 months post infection (Donadio et
al., 2022). After progression to clinical TB, meerkats usually become
terminally ill with open lesions at affected lymph nodes and die within
several months, with no recovery once clinical stage was reached
(Patterson et al., 2021). Thus, TB was reported to impact life history
and survival, and can lead to group extinctions (Duncan et al., 2021), a
pattern aggravated by climate change (Paniw et al., 2022).

Despite some detailed knowledge gained from previous cross-sectional
studies regarding TB in meerkats (summarized in Table 1), the dynamics
around its spread across the population, and how TB disease manifests
over a meerkats' lifetime, remain obscure (see Supplementary Table 1).
To fill these gaps, we leverage an extensive long-term dataset with over
25 years of detailed individual data (n= 3,420 individuals) to examine
TB spread across the population. Specifically, we quantify TB exposure,
prevalence of clinical TB, and mortality, provide timelines of typical
disease progression in individuals and groups and describe
inter-individual and temporal variation in TB progression. These
findings provide crucial context by which to understand TB epidemiology
and ecology.

\textbf{Materials and Methods}

Data used for this study was collected within the KMP on wild meerkats
living at the Kuruman River reserve (26\selectlanguage{ngerman}° 580' S, 21°490' E), Northern
Cape, South Africa, between the between the 20\textsuperscript{th} of
October 1993 and the 29\textsuperscript{th} of December 2020. During
this time, several meerkat groups well habituated to human observers
were visited multiple times a week and detailed data on individually
recognizable individuals collected by trained volunteers and researchers
following standardized protocols (for details see Clutton-Brock and
Manser, 2016). We included data on all 3,420 individuals encompassed in
the study for individual level analyses. As it is common for newly
founded meerkat groups to quickly fail (Duncan et al., 2021), we limited
the analyses on the group level to 91 groups with a group duration
longer than 6 months.

For each individual, we recorded first date as birthdate or first entry
date into the population and final date as death date or last observed
date as well as available information on clinical signs of TB infection
(see Table 2 for definitions on terminology). Individuals can be
infectious even prior to the onset of clinical signs (Wilkinson et al.,
2000; Donadio et al., 2022), and exposure can vary with social behaviour
(Drewe, 2010; Drewe et al., 2011), so exact time of exposure for each
individual cannot easily determined. However, individuals with overt
signs are likely contributing the most to TB transmission (McDonald et
al., 2019), and most individuals were either born into a TB afflicted
group or came into contact with TB upon immigration into a TB afflicted
group (see below). We consequently chose contact with visibly TB
afflicted conspecifics as a conservative, clearly identifiable and
relatively accurate estimate for TB exposure, despite some remaining
uncertainty regarding individual exposure dates. Individuals were thus
classified as TB exposed from the first day of contact to conspecifics
with externally visible signs of clinical TB, either by clinical TB
emerging in the resident group or by immigrating into a group with
visibly infected individuals. Individuals were considered presenting
clinical signs from the date they were recorded with TB by observers or
displayed clear signs of TB infection (submandibular, inguinal or
cervical lumps). If individuals had records of suspected TB, i.e. lumps
or swelling with no alternative explanation, and progressed to develop
clinical TB, the date of first putative TB symptoms was considered as
onset of clinical TB. Clearance of clinical TB has not been recorded in
meerkats, so we considered TB infections to be purely progressive with
no return to prior states (Patterson et al., 2021). Within KMP,
terminally ill individuals were euthanized to curb the spread of the
disease (Patterson et al., 2021; Duncan et al., 2021), with infections
being confirmed in post-mortem examinations (Patterson et al., 2021). We
classified these individuals as having died of TB and included them in
our dataset of TB progression (see Table 2), as terminally ill
individuals do not recover and are expected to die within a few days or
weeks (Patterson et al., 2021). To be conservative in our
interpretations, individuals displaying clinical signs at time of death
but dying of other or unknown causes (e.g. predation or disappearance)
were not considered as having died of TB. At the group level, groups
were considered as TB exposed upon the first observation of a clinically
ill individual within the group. Groups that did not persist until the
end of the study are considered extinct, irrespective of the reason of
group termination (group abandoned, disintegrated, etc.).

Based on this data, we calculated time from being exposed to developing
clinical signs as proxy of TB-susceptibility, i.e. the risk to become
clinically ill upon exposure, and time between clinical signs and death
as proxy of resistance, i.e. the capacity of a clinically ill individual
to survive despite disease. We also calculated survival (i.e. time from
exposure to death) for all exposed individuals (see Donadio et al. 2022,
see Table 2). To assess TB exposure and prevalence as well as
progression and mortality, we calculated overall and yearly proportion
of exposure, clinical infection and TB related death at the group and
individual level. Plus, the temporal patterns of TB progression, i.e. TB
susceptibility, resistance and survival (definitions see Table 2), were
analyzed. Data was retrieved from the KMP database into R using the
package RMariaDB (Müller et al., 2020) and processed using the packages
tidyverse (Wickham et al., 2019). All analyses were performed in R,
version 3.6.3 (R Core Team, 2019). Research for this study was conducted
with permission of the ethical committee of Pretoria University and the
Northern Cape Conservation Service, South Africa (Permit number:
EC031-13, FAUNA 1020-2016).

\textbf{Results}

TB was first recorded in the late 1990s in this population and spread
within \textasciitilde{} 8 years amongst all social groups and exposing
most individuals to the disease. Between 1993 and 2020, 71\% of all
individuals were exposed to TB at some point during their life (n =
2,427/3,420). The proportion of individuals exposed varied markedly
between study years (mean ± SD: 54.8 ± 38.4\%), with no TB exposure
recorded prior to 1997. Exposure levels proceeded to rise rapidly until
70 -- 95\% of individuals were exposed in any given year after 2006 and
remained at comparably high levels thereon after. In contrast, clinical
signs of the disease increased in frequency less steeply. Between 0 to
29.4\% of the study population showed clinical signs (mean ± SD: 8.6 ±
9.0\%, with 0 to around 6\% of individuals dying with confirmed TB (mean
± SD: 4.2 ± 4.6\%) in any given year (Figure 1, Supplementary Figure 1).

Individuals were most often exposed at birth (75.3\%, n = 1827), or upon
development of TB signs in their current resident group (19.8\%, n =
472). The remaining exposed individuals immigrated into a group already
experiencing TB (5.4\%, n = 128). Only 22.9\% of exposed individuals (n
= 555), corresponding to 16.1\% of the study population, developed
clinical signs of TB within 1.5 years (mean ± sd: 520 ± 421 days). The
majority of individuals reported with clinical signs were confirmed to
have died with or from TB (n = 398), leading to a TB-related mortality
rate of 11.6\% in the population. This does not account for individuals
infected, but not showing overt signs of TB, so it is likely this figure
underestimates the real extent of TB related mortality.

We observed marked inter-individual variation in TB progression and
outcomes, with time between exposure and first clinical signs ranging
from 0 (for index cases in a group) to 2,971 days (Figure 2, Figure 3).
The mean duration between exposure and signs was \textasciitilde{}1.4
years (mean ± SD: 520 ± 421 days, median: 440 days). Individuals
survived the onset of clinical signs for up to 2,756 days, although some
individuals were recorded with signs only at the time of their death. On
average, individuals survived the onset of clinical TB for
\textasciitilde{}6.6 months (mean ± SD: 200 ± 328, median: 70 days),
indicative of the rapid progression of TB after development of clinical
signs (Figure 2, Figure 3, Supplementary Figure 2). Comparing exposed
individuals progressing to clinical TB with exposed individuals never
developing TB signs, we found high variation in survival in both groups:
Individuals developing TB signs survive between 5 and 3,541 days (mean ±
SD: 720 ± 529, median = 603 days) past exposure, asymptomatic
individuals survived up to 4,123 days (mean ± SD 432 ± 485, median = 269
days) past exposure. Asymptomatic individuals thus seemed to die
significantly earlier (MWU-test: U = 723844, p \textless{} 0.001).

On the group level, we focused on 91 meerkat groups lasting between 196
and 9,235 days (mean ± SD: 1,513 ± 1,935 days, median: 660 days).
Individuals with clinical TB were present in 62 (68.1\%) groups, only
eight of which persisted until the end of the study. Additional four
groups present at the end of the study had not been in contact with TB.
TB prevalence among groups varied between 0\% before TB detection in the
study and 96\% in 2013 and 2016, with an average of 59.5 ± 33.9\% of
groups exposed to TB (Figure 1). TB was present in most groups that did
not persist (n = 54, 68.4\% of extinct groups).

After the first detection of clinical TB, groups persistence varied
between only 46 and 6356 days (mean ± SD: 1,200 ± 1,352 days, median:
569 days) and notably the two longest surviving groups in our dataset
persisted despite being exposed to TB since \textasciitilde{} 17 and 21
years, respectively. Marked variation in group survival past TB exposure
is retained when only considering groups that disintegrated after
detection of TB, after which these groups survived up to 8,243 days
(mean ± SD: 1,591 ± 1,858 days, median: 573 days).

\textbf{Discussion}

Using a large long-term dataset including over 3,400 individuals and
spanning 27 years, we report the spread of TB in wild meerkats, and
quantify the extent of TB exposure, clinical TB prevalence and
TB-related mortality. We show that exposure to TB rose to over 50\%
within approximately eight years after first detection within the
population and increased to up to over 90\%. Rates of clinical disease
and mortality over the same period peaked at around 25\% and 6\%,
respectively, suggesting a degree of resistance to the pathogen. TB
prevalence varied strongly between the years, with over one quarter of
the population displaying clinical signs in some years. TB prevalence
reported this study is comparable with those reported from other
well-studied species (\textasciitilde{} 12 \% for European badgers
(\emph{Meles meles} ) to \textasciitilde{} 32\% for red deer
(\emph{Cervus elaphus} ) and wild boar (\emph{Sus scrofa} ), see Reis et
al., 2021), both with regard to overall (16.2\%) and annual prevalence.
Previous studies, using diagnostic tools on subset of the study
population to detect TB reported prevalence between 24\% (Drewe, 2010)
and up to 82.4\% of individuals of exposed groups (Clarke et al., 2016),
implying that by using clinical signs, the true extent
of\emph{Mycobacterium} infection prevalence is underestimated.

In line with previous studies, we find TB contributing strongly to
meerkat mortality, both on the individual and group level (Patterson et
al., 2017; Duncan et al., 2021). At 11.6\%, individual TB related
mortality is almost twice as high as previously reported in the same
population (Patterson et al., 2017), and comparable with estimated
annual mortality of mongooses infected with \emph{M. mungi} (Fairbanks
et al., 2014). Most individuals (71.7\%) with clinical signs were
confirmed to have died of or with TB, yet given the irreversible nature
of TB progression, the disease was likely a contributing factor in the
death of diseased individuals dying of other causes. As many infected
individuals likely die before progressing to clinical stages,
subclinical infections are known to increase mortality risk (Patterson
et al., 2021), and the impact of \emph{Mycobacterium} infections on the
population is likely even higher than reported here.

We observe a high extend of variation of TB susceptibility, resistance
and progression patterns across the study population. Only
\textasciitilde{}22\% of exposed individuals progress to clinical TB, on
average within 1.4. years of exposure. Our findings confirm the
generally long latent or subclinical period of \emph{M.
suricattae}infections(Drewe, Dean et al., 2009; Donadio et al., 2022),
with individuals developing TB signs as long as 8 years past first
exposure. As infection occur on average 1 year before the onset of
clinical signs (Donadio et al. 2022), most exposed individuals are
likely infected for most of the time between exposure and clinical TB
manifestation. The rate of individuals not susceptible to TB has been
estimated at around 25.8\% in a recent study (Donadio et al. 2022),
implying that \textasciitilde{} 50\% of exposed individuals are infected
without displaying overt symptoms. This finding is comparable to results
in badgers, where up to 80\% of infected individuals do not present
visible TB lesions (Gallagher and Clifton-Hadley, 2000).

After onset of clinical TB, meerkats in our study died on average within
\textasciitilde{} 6.6 months, confirming the rapid progression to
terminal stages reported by previous studies of the same population
(Patterson et al., 2021; Donadio et al., 2022). This pattern of
prolonged subclinical or latent infection with rapid progression upon
onset of clinical signs is a common feature of wildlife TB (Alexander et
al., 2010; Tomlinson et al., 2013; Spickler, 2019). Individuals survived
for up to 7.5 years post first TB signs, suggesting factors facilitating
natural TB resistance. The capacity of some individuals to survive TB
for a long period is another common feature of wildlife MTC pathogen
infections (Ezenwa et al., 2010; Tomlinson et al., 2013). Paradoxically,
individuals eventually developing TB signs die at older ages than
individuals that never proceed to clinical TB stages, a phenomenon most
likely attributable to the long latent period compared to meerkat life
expectancy. Baseline mortality rates in meerkats are high, with
subordinates suffering increased mortality risk upon evictions (Cram et
al., 2018), so while KMP meerkats can live up to \textasciitilde{}12
years, median life expectancy is only 2.3 years (Drewe, 2009), making
death of infected individuals prior to clinical manifestation of TB a
likely occurrence.

The origin of \emph{M. suricattae} in the study population and when it
first emerged is currently unclear. Furthermore, whether meerkats are
the original host, or the pathogen was transmitted from another, yet
unknown reservoir species, is not clear to date (Alexander et al., 2010;
Parsons et al., 2013). While the disease was probably present in the
study population from the beginning of data recording, and exposure as
well as prevalence are likely underestimated in the first years of the
long-term project, clinical TB is a highly conspicuous and easily
recognizable disease, allowing the conclusion that the rapid increase in
detected cases after the late 1990s is reflective of increased disease
prevalence and transmission rather than an artifact of observation bias.
This conclusion is also supported by the observation that both bovine
and non-bovine TB seems to become increasingly prevalent in southern
Africa (Michel et al., 2006; Alexander et al., 2010; Tanner et al.,
2015; Parsons et al., 2019). Originally, inter-species transmission
of\emph{M. bovis} was suspected to cause the TB outbreaks in meerkats
(Drewe, Dean et al., 2009; Drewe, Foote et al., 2009) before
identification of \emph{M. suricattae} (Parsons et al., 2013, 2019),
which is now considered to be endemic in meerkats (Patterson et al.,
2022).

The mechanisms underlying this increased TB prevalence and transmission
are likely complex and multi-faceted, and their detailed discussion is
beyond the scope of this study. However, based on our findings and
previous research, we can identify factors that likely contributed to
the rapid spread of TB, both inherent to the host-pathogen system and
external factors, and discuss the implication of the establishment of TB
within the population. Even though clinical TB is highly contagious,
there are no obvious behavioural defenses against TB transmission in
meerkats: Banded mongooses (\emph{Mungos mungo} ), which are closely
related to meerkats, apparently do not avoid TB affected conspecifics
(Fairbanks et al., 2015), and there is no evidence for avoidance
behaviour in meerkats to date. Additionally, subclinically infected
individuals have been shown to shed \emph{M. suricattae} via their
faeces (Donadio et al., 2022) and thus might be infectious and
facilitate transmission, as observed in badgers (Graham et al., 2013;
Tomlinson et al., 2013). Both factors could favour spread of TB within a
susceptible population. Both within and between group social contact
patterns are well established as contributing factors to TB transmission
in social mammals (Drewe, 2010; Weber et al., 2013), and in meerkats in
particular, migrating males have been implicated to transmit TB between
groups (Duncan et al., 2021; Paniw et al., 2022). Consequently, long
subclinical infection periods, limitations in behaviourally avoiding TB
exposure, and frequent social contacts can facilitate rapid TB
transmission within a population based on high levels of exposure.

Transmission can further be facilitated by increased susceptibility to a
pathogen. Adverse climate conditions have been suggested to exacerbate
the negative effects of TB on individuals and populations (Dwyer et al.,
2020; Paniw et al., 2022), potentially indicative of such increased
susceptibility to TB of individuals affected by environmental stressors.
In the study population, above average temperatures increasingly
occurred after the early 2000s and correlate with clinical TB occurrence
(Paniw et al., 2022). Both, adverse climate conditions and clinical TB
reduce meerkat survival and can lead to group failure, particularly of
small groups (Duncan et al., 2021; Paniw et al., 2022), which can lead
to higher social mobility, as remnant individuals form new groups or
immigrate into other groups. With immigration increasing the risk of TB
transmission into previously TB-free groups, these may become more
vulnerable to adverse environmental conditions and group extinction once
individuals progress to clinical TB and the group suffers from TB
related mortality (Duncan et al., 2021; Paniw et al., 2022). Thus, the
negative effects of climate change and TB emergence can enforce each
other, facilitating TB transmission throughout the study population and
affecting population dynamics. Potentially, the effect of \emph{M.
suricattae} infections transcends meerkats and has implications for
entire eco-systems, based on the high inter-species transmissibility of
MTC pathogens and a wide TB presence in South African mammals (Hlokwe et
al., 2014; Clarke et al., 2016; Parsons et al., 2019). Predation is one
of the main causes of meerkat mortality (\textasciitilde{}25\%, NMK,
unpublished data), so meerkat predators are likely to become exposed
to\emph{M. suricattae} via infected prey, potentially facilitating
transmission via ingestion. This possibility highlights the need for
detailed and systematic surveillance studies to understand the impact of
TB on not only single species, but entire ecosystems.

Our study is based on purely observational data and thus not suitable to
investigate determinants of TB susceptibility, resistance and
progression. Individuals differ strongly in how they are affected by TB,
and the high level of exposed but never clinically ill individuals is
suggestive of non-susceptible individuals within the population. Future
studies should investigate the impact of hosts immune genetics and
responses ( Ezenwa and Jolles, 2015; Ezenwa et al., 2021; Jolma et al.,
2021; Marjamäki et al., 2021) in explaining the variation in TB
susceptibility, resistance and progression. Furthermore, assessing for
effects of pathogen-mediated selection on meerkat population genomics
and risk of co-infections will be highly informative furthering our
understanding of the effect of TB on meerkat ecology and evolution.

\textbf{Acknowledgements}

We thank Dr. Pablo Santos for his invaluable support during an early
stage of the project and Dr. Stuart Patterson for his mindful comments
on the manuscript. We are grateful to the Kalahari Research Trust and
the Kalahari Meerkat Project for access to facilities and habituated
animals in the Kuruman River Reserve, South Africa. This paper has
relied on records of individual identities and/or life histories
maintained by the Kalahari Meerkat Project, which has been supported by
the European Research Council (ERC) under the European Union's Horizon
2020 research and innovation programme (Research Grant Nos 294494 and
742808 to T.H. Clutton-Brock since 1/7/2012), the Human Frontier Science
Program (funding reference RGP0051/2017), the University of Zurich, the
Swiss National Science Foundation and the Mammal Research Institute at
the University of Pretoria, South Africa. Research for this study was
conducted with permission of the ethical committee of Pretoria
University and the Northern Cape Conservation Service, South Africa
(Permit number: EC031-13, FAUNA 1020-2016). The study is funded by the
German Research Foundation to S. Sommer (DFG SO 428/15-1).

\textbf{Conflict of interest statement}

The authors declare no conflicts of interest

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\textbf{Tables and Figures}

Table 1. Previous studies on \emph{Mycobacterium} infections in wild
meerkats in the Kalahari, South Africa with highlighted key findings.\selectlanguage{english}
\begin{longtable}[]{@{}lllll@{}}
\toprule
Reference & Study type & Data collection & Sample size & Key
findings\tabularnewline
\midrule
\endhead
Alexander et al., 2002 & Pathogen identification & 1998/1999 & N = 20 &
Immigration of TB afflicted individual followed by development of signs
and death/ disappearance of all group members\tabularnewline
Drewe, Foote et al., 2009 & TB pathology & 2005 - 2007 & N = 57 &
Detailed pathology of 52 individuals euthanized for TB, lesions in
multiple organ systems\tabularnewline
Drewe, Dean et al., 2009b & TB detection assay validation & 2005 - 2007
& N = 240 & Combining multiple diagnostic tools increases TB detection
reliability\tabularnewline
Drewe 2010 & TB transmission study & 2006/2007 & N = 110 & TB
transmission is impacted by social network parameters. Giving grooming
and receiving aggression main risk factors\tabularnewline
Drewe et al., 2011 & TB transmission study & 2006/2007 & N = 134 & TB
transmission impacted by social network parameters. Exposure driven
mainly by grooming interactions\tabularnewline
Parsons et al., 2013 & Molecular description of TB & Not reported & N =
4 & Identification and description of \emph{M. suricattae,} closely
related to \emph{M. mungi} and dassie bacillus\tabularnewline
Clarke et al., 2016 & TB detection assay validation & 2014/2015 & N=108
& IP-10 release assay as viable method of TB detection in
meerkats\tabularnewline
Patterson et al., 2017 & TB transmission study & 2001 - 2015 & N = 2388
& TB infection risk increased by older age, group history of TB, prior
immigration into social group\tabularnewline
Patterson et al., 2021 & TB detection assay validation & 2014 - 2016 & N
= 268 & TB infections double mortality risk; combining multiple
diagnostic tools increases TB detection reliability\tabularnewline
Patterson et al., 2022 & Intervention study & 2014 - 2016 & N = 135 &
Vaccinations of high contact individuals or highly susceptible
individuals reduces TB infection rates\tabularnewline
Duncan et al., 2021 & TB effect on demography & 1993 - 2019 & N = 98
groups & TB linked to group failure, prior immigration into social group
increases TB risk\tabularnewline
Paniw et al., 2022 & TB effect on demography & 1997 - 2018 & N = 2691 &
Impact of adverse climate exacerbated by TB, prior immigration into
social group increases TB risk\tabularnewline
Donadio et al., 2022 & TB detection assay validation & 1998 - 2018 & N =
66 & Detection of \emph{M. suricattae} from faeces viable, marked
variation in disease progression\tabularnewline
Present study & Quantification of TB & 1993 - 2020 & N = 3420 & High
levels of TB exposure, marked variation in TB progression\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 2.} TB related terminology and definitions of life-history
parameters used in the present study.\selectlanguage{english}
\begin{longtable}[]{@{}lll@{}}
\toprule
Term & Definition & Definition\tabularnewline
\midrule
\endhead
TB classification & TB classification & TB classification\tabularnewline
Exposure & Meerkats are classified as exposed to TB if they a) are
cohabiting with an individual expressing clinical signs of TB, b) are
born into a group with past or ongoing TB history. The exposed status
does not change if individuals e.g. emigrate and enter a TB-free group,
rather it signifies a high likelihood that individuals had contact with
\emph{M. suricattae} at some point in their life. Exposed individuals
may be infected, but do not (yet) express clinical signs. & Meerkats are
classified as exposed to TB if they a) are cohabiting with an individual
expressing clinical signs of TB, b) are born into a group with past or
ongoing TB history. The exposed status does not change if individuals
e.g. emigrate and enter a TB-free group, rather it signifies a high
likelihood that individuals had contact with \emph{M. suricattae} at
some point in their life. Exposed individuals may be infected, but do
not (yet) express clinical signs.\tabularnewline
Clinical TB signs & Meerkats are classified as clinical TB cases from
the first day they express clear signs of \emph{M. suricattae}
infection, specifically lymphadenopathy of submandibular, cervical or
inguinal lymphnodes, or when they were classified as displaying TB signs
by field observers. Individuals with clinical TB are exposed by
definition. & Meerkats are classified as clinical TB cases from the
first day they express clear signs of \emph{M. suricattae} infection,
specifically lymphadenopathy of submandibular, cervical or inguinal
lymphnodes, or when they were classified as displaying TB signs by field
observers. Individuals with clinical TB are exposed by
definition.\tabularnewline
Group TB & Past or present cases of clinical TB within the respective
group. Based on the long subclinical phases, individuals in groups with
past, but not current clinical TB, are considered exposed to TB. Current
clinical cases are not required for a group to be defined as a group
with TB cases. & Past or present cases of clinical TB within the
respective group. Based on the long subclinical phases, individuals in
groups with past, but not current clinical TB, are considered exposed to
TB. Current clinical cases are not required for a group to be defined as
a group with TB cases.\tabularnewline
Susceptibility & The time taken for an exposed meerkat to develop
clinical signs of TB, used as proxy of individual susceptibility to
\emph{M. suricattae} infection upon exposure. While disease transmission
is determined by both exposure and susceptibility to a pathogen, the
susceptibility term here encompasses both mechanisms, so `exposure' can
be used to describe whether individuals are considered in contact with
\emph{M. suricattae}. & The time taken for an exposed meerkat to develop
clinical signs of TB, used as proxy of individual susceptibility to
\emph{M. suricattae} infection upon exposure. While disease transmission
is determined by both exposure and susceptibility to a pathogen, the
susceptibility term here encompasses both mechanisms, so `exposure' can
be used to describe whether individuals are considered in contact with
\emph{M. suricattae}.\tabularnewline
Resistance & The time-period between development of clinical signs and
death, representing the capability of an individual to withstand
negative effects of the infection. Please note that here, the term
resistance is not referring to immune function or implying the nature of
immune responses of the individual against \emph{M. surciattae} but
signifies individual capacity to survive with clinical TB. & The
time-period between development of clinical signs and death,
representing the capability of an individual to withstand negative
effects of the infection. Please note that here, the term resistance is
not referring to immune function or implying the nature of immune
responses of the individual against \emph{M. surciattae} but signifies
individual capacity to survive with clinical TB.\tabularnewline
Survival & Time period between exposure to TB and death, irrespective of
development of clinical disease. & Time period between exposure to TB
and death, irrespective of development of clinical
disease.\tabularnewline
TB death & Individual was euthanized with terminal TB infection or
infection was confirmed by post-mortem examination. Individuals
clinically ill with TB but dying of other causes are not included here.
& Individual was euthanized with terminal TB infection or infection was
confirmed by post-mortem examination. Individuals clinically ill with TB
but dying of other causes are not included here.\tabularnewline
Life history parameters & Life history parameters &\tabularnewline
First date & First recorded date for the respective individual, i.e.
birthdate for individuals born into the study population, or date of
first inclusion in the study in case of newly habituated or immigrated
individuals. & First recorded date for the respective individual, i.e.
birthdate for individuals born into the study population, or date of
first inclusion in the study in case of newly habituated or immigrated
individuals.\tabularnewline
Last date & Last recorded date for the respective individual, i.e. date
of death or last record of the individual before disappearance. & Last
recorded date for the respective individual, i.e. date of death or last
record of the individual before disappearance.\tabularnewline
Group start & First date of records for the respective group & First
date of records for the respective group\tabularnewline
Group end & Recorded date of group failure, irrespective of the nature
of this failure (group split, group extinction or group abandoned). &
Recorded date of group failure, irrespective of the nature of this
failure (group split, group extinction or group
abandoned).\tabularnewline
\bottomrule
\end{longtable}

\textbf{Figure 1}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 1:} Patterns of TB exposure, prevalence of clinical signs
and TB-related death over 27 years of research at the Kalahari Meerkat
Project (South Africa) illustrating the inter-annual variation and
development of TB prevalence within the study population. Absolute
numbers (barplots) and proportion of A) meerkat groups and B)
individuals of the study population being not exposed yet (green),
exposed (blue), displaying clinical signs of TB (orange) or dying with
confirmed TB (red). Means \selectlanguage{ngerman}± sd of each measure were calculated in
3-months increments.

\textbf{Figure 2}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

\textbf{Figure 2:} Life trajectories of meerkats that developed clinical
TB (n = 555). For each individual, respective first (birth or entering
into the study population) and last (death or disappearance) dates, as
well as transitions between TB states are shown. Individuals were on
average exposed to TB for 1.4 years before the onset of clinical signs
and survived on average until 6.6 months after developing clinical TB.
Individuals are sorted by birth date.

\textbf{Figure 3}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

\textbf{Figure 3:} Meerkat life expectancy. Variation in life expectancy
of meerkats with known final age (i.e. age at death or disappearance, n=
3,113), based on their TB status. Points indicate the mean, vertical
lines the standard deviation.

\textbf{Supplementary Material}

Supplementary Table 1. Summary of information available on
\emph{Mycobacterium infections} in wild meerkats in the Kalahari, South
Africa.\selectlanguage{english}
\begin{longtable}[]{@{}lllllllll@{}}
\toprule
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB prevalence\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Reference\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Exposure}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Clinical TB signs}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Confirmed TB infection}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Mortality}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{TB detection}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Sample size}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Data collection}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Comments}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Alexander et al., 2002\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
100\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
100\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 1\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
100\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs, PM, MC\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 20\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
1998/1999\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Tracking TB spread through 1 group following immigration of positive
individual\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Drewe, Foote et al., 2009\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
91.2\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
91.2\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
91.2\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
PM, MC\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 57\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2005 - 2007\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Detailed pathology of 52 individuals euthanized for TB (5 individuals as
control)\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Drewe, Dean et al., 2009\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
46.7\%*\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
13.2\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
MC, IRT\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 240\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2005 - 2007\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Exposure determined by immune-reaction assay\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Drewe 2010\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
9\% to 33\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
MC, IRT\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 110\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2006/2007\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB transmission study, prevalence reported in 3 months periods\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Drewe et al., 2011\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
30\%*\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
MC, IRT\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 134\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2006/2007\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Exposure determined by immune-reaction assay, longitudinal testing of 37
individuals\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Clarke et al., 2016\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
34.7\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
IRT\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N=108\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2014/2015\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB detected by immune-reaction assay, 24.7\% to 82.4\% depending on
estimated exposure risk\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Patterson et al., 2017\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
6\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
6\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
6\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 2388\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2001 - 2015\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB defined as clinical signs followed by TB related euthanasia\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Patterson et al., 2021\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
17.5\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
8.95\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
11.1\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
PM, MC, IRT, PCR\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 268\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2014 - 2016\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB detection assay validation\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Patterson et al., 2022\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
19\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
MC, IRT\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 135\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2014 - 2016\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Intervention study\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Duncan et al., 2021\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
63\% (group level)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
63\% (group level)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 98 groups\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
1993 - 2019\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB effect on demography\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
Donadio et al., 2022\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
100\%\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
56.1\%\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
60.6\%\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
27.3\%\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
Signs, PCR\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
N = 66\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
1998 - 2018\strut
\end{minipage} & \begin{minipage}[t]{0.11\columnwidth}\raggedright\strut
TB detection assay validation; individuals selected for likely TB
exposure and signs; TB infections: 53\% signs + PCR, 7.6\% PCR
only\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
present study\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
71\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
16.1\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
11.6\%\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 3420\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
1993 - 2020\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
TB quantification\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
B) TB progression\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Reference\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Exposure -- infection}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Exposure - signs}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Infection - signs}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Signs - death}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{TB detection}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Sample size}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Data collection}\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textbf{Comment}\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Alexander et al., 2002\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textasciitilde{}6 and 14 m\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs, PM, MC\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 20\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
1998/1999\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
See above\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Drewe 2010\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
10m (1.5-25.3m)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
MC, IRT\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 110\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2006/2007\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
See above\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Drewe et al., 2011\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
12.6m\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
8.1m (infection to death)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
MC, IRT\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 134 (37 longitudinal testing)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2006/2007\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
See above\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Patterson et al., 2017\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
\textless{} 6 months\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs, TB related euthanasia\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 2388\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
2001 - 2015\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
See above\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Duncan et al., 2021\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
10 months (group level)\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 98 groups\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
1993 - 2019\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
See above\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Donadio et al., 2022\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
14.0 \selectlanguage{ngerman}± 10.8m\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
11.5 \selectlanguage{ngerman}± 6.9m\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
5.3 \selectlanguage{ngerman}± 5.7m\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs, PCR\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 66\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
1998 - 2018\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
See above\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Present study\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
17.1 \selectlanguage{ngerman}± 13.8m\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
n.r.\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
6.6 \selectlanguage{ngerman}± 10.8m\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Signs\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
N = 3420\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
1993 - 2020\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
See above\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage} & \begin{minipage}[t]{0.08\columnwidth}\raggedright\strut
Abbreviations: PM: post mortem examination; signs: clinical signs of TB;
MC: Mycobacterial cultures; IRT: Immune response tests; n.r.: not
reported *Positive in immune reaction assays For all studies, durations
reported in days were transformed into months to allow easier comparison
between studies\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}



\textbf{Supplementary Figure 1}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image4/image4}

\end{center}
\end{figure}

\textbf{Supplementary Figure 1:} Patterns of TB exposure, prevalence of
clinical signs and TB-related death over 27 years of research at the
Kalahari Meerkat Project (South Africa) illustrating the inter-annual
variation and development of TB prevalence within the study population.
The numbers of A) study groups and B) study individuals of the study
population being not exposed yet (green), exposed (blue), displaying
clinical signs of TB (orange) or dying with confirmed TB (red). Means \selectlanguage{ngerman}±
sd of each measure were calculated in 3-months increments.

\textbf{Supplementary Figure 2}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image5/image5}

\end{center}
\end{figure}

\textbf{Supplementary Figure 2:} Life trajectories of meerkats (n =
3,420). For each individual, respective first (birth or entering into
the study population) and last (death or disappearance) dates, as well
as transitions between TB states are shown. Individuals were on average
exposed to TB for 1.4 years before the onset of clinical signs and
survived on average until 6.6 months after developing clinical TB.
Individuals are sorted by birth date.\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-1/Figure-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Supplement-Figure-1-1/Supplement-Figure-1-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Supplement-Figure-1-2/Supplement-Figure-1-2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2/Figure-2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Supplement-Figure-2/Supplement-Figure-2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-3/Figure-3}

\end{center}
\end{figure}

\selectlanguage{english}
\FloatBarrier
\end{document}

